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Because horned animals are prone to conflict, they may have a higher risk of developing a brain contusion as a result of a horn strike. Repeated brain trauma can affect the hippocampus, which is involved in memory and orientation. The aim of this study was to histopathologically examine the blood-brain barrier (BBB) of the hippocampus in horned and hornless female sheep. Skulls of 4 horned and 6 hornless female sheep aged 16±4 months were obtained from the abattoir. Brains were carefully removed and preserved in 10 % formalin for 5 days. Sections were taken from bilateral hippocampus. Specimens were stained with hematoxylin-eosin (H&E) and Tunel methods, and the histopathologic structures of the BBB were examined by light microscopy. BBB damage scores evaluated. The results were analyzed by Mann-Whitney U test. The BBB damage score was found to be higher in horned female sheep. Astrocytes was more branching and BBB was more intact in hornless female sheep. This is considered that more astrocyte branches may play an important role in the protective mechanism. The difference in intracerebral defense mechanism against brain trauma in female sheep may serve as a model for investigating molecular mechanisms. The impairment of the BBB in the hippocampal region of horned female sheep may result in their memory, intelligence, and navigational abilities being lower than those of hornless female sheep. This could open the horizon for better advances in human and animal brain health. [ABSTRACT FROM AUTHOR]

Formaldehyde induces oxidative damage in hippocampal tissue and blood serum by suppressing antioxidant defenses and increasing lipid peroxidation. This results in damage to DNA, proteins, and lipids within cells, disrupting neuronal functions, and may even lead to cell death (apoptosis). Apoptosis occurs as a cellular response triggered by formaldehyde through various mechanisms, including mitochondrial dysfunction, oxidative stress, and DNA damage. Arbutus unedo L. (AUL), which is rich in antioxidants, represents a potential countermeasure. The aim of our study is to investigate the immunohistochemical and biochemical effects of AUL fruit extract (AUE) on apoptosis and oxidative stress induced by FA exposure in the rat hippocampus. The rats were divided into four groups: the experimental group (EG) received 20 mg/kg AUE by oral gavage and 10 ppm FA inhalation; the formaldehyde group (FG) received 10 ppm FA inhalation only; the sham group (SG) received 10 mg/kg AUE by oral gavage; and the control group (CG) underwent routine observation. Hippocampal tissue was isolated after blood sampling. A number of physical changes, such as yellowing of feathers and tail spots, were observed in FA-exposed groups. The biochemical analysis showed significant differences in brain-derived neurotrophic factor (BDNF), malondialdehyde (MDA), GSH (Glutathione) and nitric oxide (NO) levels between the groups. The AUE-treated groups had reduced MDA levels, suggesting a potential reduction in oxidative stress, along with lower apoptotic cell rates in caspase-3 assessments. The FG rats had lower BDNF levels than CG. The SG had the fewest apoptotic cells. All these findings indicate AUE's potential to mitigate neuron damage and reduce oxidative stress. [ABSTRACT FROM AUTHOR]

Introduction: Pituitary adenylate cyclase-activating polypeptide (PACAP) regulates plasticity in brain systems underlying arousal and memory and is associated with posttraumatic stress disorder (PTSD). Research in animal models suggests that PACAP modulates entorhinal cortex (EC) input to the hippocampus, contributing to impaired contextual fear conditioning. In PTSD, PACAP is associated with higher activity of the amygdala to threat stimuli and lower functional connectivity of the amygdala and hippocampus. However, PACAP-affiliated structural alterations of these regions have not been investigated in PTSD. Here, we examined whether peripheral PACAP levels were associated with neuronal morphology of the amygdala and hippocampus (primary analyses), and EC (secondary) using Neurite Orientation Dispersion and Density Imaging. Methods: Sixty-four (44 female) adults (19 to 54 years old) with DSM-5 Criterion A trauma exposure completed the Clinician-Administered PTSD Scale (CAPS-5), a blood draw, and magnetic resonance imaging. PACAP38 radioimmunoassay was performed and T1-weighted and multi-shell diffusion-weighted images were acquired. Neurite Density Index (NDI) and Orientation Dispersion Index (ODI) were quantified in the amygdala, hippocampus, and EC. CAPS-5 total score and anxious arousal score were used to test for clinical associations with brain structure. Results: Higher PACAP levels were associated with greater EC NDI (β = 0.0099, q = 0.032) and lower EC ODI (β = −0.0073, q = 0.047), and not hippocampal or amygdala measures. Neither EC NDI nor ODI was associated with clinical measures. Conclusions: Circulating PACAP levels were associated with altered neuronal density of the EC but not the hippocampus or amygdala. These findings strengthen evidence that PACAP may impact arousal-associated memory circuits in PTSD. [ABSTRACT FROM AUTHOR]

Background: High-quality friendships have a positive impact on the mental health of young people with childhood adversity (CA). Social stress buffering, the phenomenon of a social partner attenuating acute stress responses, is a potential yet unexplored mechanism that may underlie this relationship. Objective: This study examined whether perceived friendship quality was related to better mental health and lower neural stress response in young people with CA. Method: A total of N = 102 young people (aged 16–26) with low to moderate CA were included in the study. We first investigated associations between friendship quality, mental health, and CA. In a representative subset (n = 62), we assessed neural stress responses using the Montreal Imaging Stress Task. In our sample, CA was best described along two dimensions resembling threat or deprivation like experiences. Hence, we investigated both cumulative and dimensional effects of CA. Results: We found no support for social thinning after CA, meaning that the severity of CA (cumulative or dimensional) did not differentially impact friendship quality. High-quality friendships, on the other hand, were strongly associated with better mental health. Furthermore, acute stress increased state anxiety and enhanced neural activity in five frontolimbic brain regions, including the left hippocampus. We found weak support that threat experiences interacted with friendship quality to predict left hippocampal reactivity to stress. However, this effect did not survive multiple comparison correction. Conclusion: The absence of social thinning in our sample may suggest that the risk of developing impoverished social networks is low for rather well-functioning young people with low to moderate CA. Regardless, our findings align with prior research, consistently showing a strong association between high-quality friendships and better mental health in young people with CA. Future research is needed to examine whether friendships aid neural stress responses in young people with childhood threat experiences. Young people with childhood adversity underwent acute stress induction, eliciting frontolimbic reactivity. High-quality friendships were strongly associated with better mental health. Weak support for friendship stress buffering did not survive multiple comparison correction. [ABSTRACT FROM AUTHOR]

Hypoxia-induced factor 1 (HIF-1) plays a fundamental role in the response to low oxygen tension, since it regulates the expression of a wide variety of genes, whose products participate in processes such as angiogenesis, energy metabolism, erythropoiesis, and cell proliferation as well as in the process of neurogenesis, which involves various stages, such as proliferation of neuronal stem cells, migration, differentiation, survival of new neurons, and integration of the same. Among the many intrinsic and extrinsic molecular signals that regulate the production of new neurons from progenitor cells in the adult in the central nervous system (CNS), hypoxic damage plays an important role in the maintenance and function of stem cells in development and disease. [ABSTRACT FROM AUTHOR]

Introduction: Facial nerve injury induces changes in hippocampal long-term synaptic plasticity and affects both object recognition memory and spatial memory consolidation (i.e., hippocampus-dependent tasks). Although facial nerve injury-associated microglial activation has been described regarding the primary motor cortex, it has not been ascertained whether something similar occurs in the hippocampus. Peripheral nerve injuryassociated microglial changes in hippocampal tissue could explain neuronal changes in the contralateral hippocampus. Objective: To characterize the effect of unilateral facial nerve injury on microglial proliferation and activation in the contralateral hippocampus. Materials and methods. Immunohistochemical experiments detected microglial cells in the hippocampal tissue of rats that had undergone facial nerve injury. The animals were sacrificed at specific times after injury to evaluate hippocampal microglial cell proliferation (cell density) and activation (cell area); sham-operated animals were compared to lesioned animals sacrificed 1, 3, 7, 21, or 35 days after injury. Results: Facial nerve-injured rats' hippocampal microglial cells proliferated and adopted an activated phenotype 3- to 21-days post-lesion. Such modifications were transient since the microglial cells returned to their resting state five weeks after injury, despite the injury's irreversible nature. Conclusions: Facial nerve injury causes the transient proliferation and activation of microglial cells in the hippocampus. This finding might partly explain the morphological and electrophysiological changes described for CA1 pyramidal neurons and the impairment of spatial memory consolidation which has previously been observed in facial nerve-injured rats. [ABSTRACT FROM AUTHOR]

Diabetes mellitus can lead to structural disorders in the brain. One of the most common complications of diabetes, diabetic neuropathy is associated with central nervous system disorders. Aloe vera has anti-diabetic, antioxidant, and neuroprotective effects. This study was designed to evaluate the effects of Aloe vera gel on the hippocampus changes as well as the expression of nerve growth factor and receptors TrkA and P75 in the hippocampus of streptozotocin (STZ)-induced diabetic rats. 25 male Wistar rats were randomly divided into 5 groups including: control (normal saline), diabetic (normal saline), Aloe vera gel (400 mg/kg/day; gavage), diabetic + Aloe vera gel (400 mg/kg/day; gavage) and diabetic + insulin NPH (10 IU/kg/day; subcutaneous). Experimental diabetes was induced by streptozotocin injection (60 mg/kg; intraperitoneal). All groups treated for 8 weeks. At the end of treatment course, the rat brains were removed for measuring the expression of nerve growth factor, p75 and TrkA receptors were evaluated in the hippocampus. Diabetes induction after 8 weeks caused NGF and P75 expression levels in the diabetic group than other groups significantly increased (p<0.05). The TrkA receptor expression in the diabetic group compared with the control had a significant reduction (p<0.05). On the other hand in the diabetic group receiving Aloe vera gel expression of NGF and P75 expression levels compared to the diabetic group was significantly reduced (p<0.05) and the TrkA receptor expression compared with the diabetic group had a significant increase (p<0.05). The results showed that oral administration of Aloe vera gel in diabetic rats ameliorates diabetes-induced hyperglycemia. On the other hand, Aloe vera gel cause modulation of the expression of NGF neurotrophic factor via increased expression of TrkA receptor-specific and non-specific receptor down-regulation of P75 in the hippocampus of STZ-induced diabetic rats. [ABSTRACT FROM AUTHOR]

Childhood trauma (CT) is associated with altered brain anatomy. These neuroanatomical changes might be more pronounced in individuals with a psychiatric disorder. Post-traumatic stress disorder (PTSD) and borderline personality disorder (BPD) are more prevalent in individuals with a history of CT. In this study, we examined limbic and total brain volumes in healthy women with and without a history of CT and in females with PTSD or BPD and a history of CT to see whether neuroanatomical changes are a function of psychopathology or CT. In total, 128 women (N = 70 healthy controls without CT, N = 25 healthy controls with CT, N = 14 individuals with PTSD, and N = 19 individuals with BPD) were recruited. A T1-weighted anatomical MRI was acquired from all participants for Freesurfer-based assessment of total brain, hippocampus, and amygdala volumes. Severity of CT was assessed with a clinical interview and the Childhood Trauma Questionnaire. Group differences in hippocampal and amygdala volumes (adjusted for total brain volume) and total brain volume (adjusted for height) were characterized by analysis of covariance. Volume of the total brain, hippocampus, and amygdala did not differ between the four groups (p >.05). CT severity correlated negatively with total brain volume across groups (r = −0.20; p =.029). CT was associated with reduced brain volume but PTSD or BPD was not. The association between CT and reduced brain volume as a global measure of brain integrity suggests a common origin for vulnerability to psychiatric disorders later in life. No group differences (healthy women with and without CT, women with BPD and CT, women with PTSD and CT) in hippocampal, amygdala, and total brain volume. Significant negative association between CT severity with total brain volume and depressive symptoms with hippocampal volumes. [ABSTRACT FROM AUTHOR]

Meta-analytic results indicate that posttraumatic stress disorder (PTSD) is associated with hypoactivation of the medial prefrontal cortex (mPFC), hyperactivation of the amygdala, and volume reductions of the hippocampus. Effective psychotherapeutic treatments were hypothesized to normalize these neural patterns via upregulation of prefrontal structures, which in turn downregulate limbic regions. To gain a sound understanding of the effects of successful psychotherapy on the brain, neural changes from pre- to post-treatment in PTSD patients will be aggregated. A systematic literature search identified 24 original studies employing structural or functional MRI measurements both before and after treatment of patients diagnosed with PTSD. In conjunction, the review returned little evidence of an activation increase in the mPFC/rostral anterior cingulate cortex (rACC) following successful treatment. Five out of 12 studies observed such an increase (especially during emotion processing tasks), albeit in partially non-overlapping brain regions. Conversely, neither the putative related activation decrease in the amygdala nor volumetric changes or altered activation during the resting state could be convincingly established. Successful psychological treatments might potentially work via upregulation of the mPFC, which thus may be involved in symptom reduction. However, the role of the amygdala in recovery from PTSD remains unclear. There is currently no indication that the various PTSD treatment approaches employed by the reviewed studies differ regarding their action mechanisms, but further research on this topic is needed. There is little evidence for an activation increase in mPFC/rACC following successful PTSD treatment. Most studies detected no significant activation changes in amygdala, insula, or hippocampus. There is no consistent evidence for post-treatment volume changes in any brain region. [ABSTRACT FROM AUTHOR]

This study aims to investigate the Effects of Titanium dioxide nanoparticles (TiO2 NPs) on the stereological parameters in the dentate gyrus and the morphology of granular hippocampal neurons in adult mice. Adult male mice (n=20, weight average: 45 g) were randomly divided into four groups including: group receiving saline (controls), low-dose (LD) 2.5 mg/kg TiO TiO2 NPs, medium-dose (MD) 5 mg/kg TiO2 NPs and high-dose (HD) 10 mg/kg TiO2 NPs, daily using gavage for 35 days. To estimate the volume of the hippocampus, dentate gyrus, and sub-layers of dentate gyrus the Cavalieri principle was used. The physical dissector was used to determine the numerical density of dentate gyrus granular cells. For analyzing the morphology of dentate gyrus granular cells the qualitative Golgi staining was used. Our data showed that the total volume of the hippocampus, dentate gyrus and its sublayers including molecular, granular and polymorph in TiO2 treated mice decreased significantly compared to the control group. Moreover, the total number and numerical density of dentate gyrus granular sub layer cells showed a significant reduction in all three experimental groups compared to the control group. The granular cells of the dentate gyrus had shorter dendritic length and decreased dendritic branches in the TiO2-treated in comparison with the control mice. These data can justify the disorders related to memory, learning and hippocampus neurons damages due to using of TiO2 NPs. [ABSTRACT FROM AUTHOR]

Accumulating evidence from preclinical and clinical studies indicates prenatal exposure to stress or excess glucocorticoids can affect offspring brain. Glucocorticoid receptor (GR) is an important target of glucocorticoid. Therefore the aim of the present study was to investigate the expression of GR in prenatally stressed adult offspring and the relationship between GR expression and behavior in offspring. Pregnant rats received restraint stress during the last week of pregnancy. Hippocampal glucocorticoid receptor expression levels in the offspring were detected on postnatal 60 (P60). Cognition function was also detected. It shows significantly lower hippocampal GR expression was observed in female prenatally stressed offspring compared with their controls at P60. Corresponding to the expression of GR, female prenatally stressed offspring exhibited poorer spatial learning and memory abilities in the Barnes maze than control, This suggests that cognitive impairment in prenatally stressed rat offspring attribute lower hippocampal GR expression. [ABSTRACT FROM AUTHOR]

Background: Numerous years of theory and research have informed our understanding of the caregiving experiences that confer vulnerability for dissociation. This work has resulted in widespread agreement on the role of childhood maltreatment as an aetiological factor. Objective: With clear integration of this perspective, the current paper draws attention to the spectrum of vulnerability that can exist over and above the trauma of maltreatment within early caregiving experiences. Method: An integrative review of the developmental literature on dissociation is presented. Results: We first review and integrate existing developmental theories of dissociation into a more unified perspective, highlighting a combination of defensive and intersubjective pathways towards dissociative outcomes. Next, we present empirical research demonstrating which specific caregiving experiences are associated with dissociation. Lastly, we review recent neurodevelopmental research demonstrating that (non-extreme) caregiving stressors during infancy impact the developing limbic structures in the brain. We conclude by offering directions for future research. Conclusion: Findings make the case for approaching assessments of the caregiver-child relationship with discernment of factors beyond the presence/absence of maltreatment when conceptualizing risk pathways toward dissociation. • Dissociation develops from infancy in the context of stressors in the caregiver-child relationship. • These stressors canoccur with, but also without maltreatment. • Changes in limbic brain regions may partly explain why such early stressors increase risk for dissociation. [ABSTRACT FROM AUTHOR]

Behavioural, structural, and functional neuroimaging have implicated the hippocampus as a critical brain region in posttraumatic stress disorder (PTSD) pathogenesis. Recent work in a normative, primarily European, sample identified 15 unique genetic loci contributing to structural variability in six hippocampal subfield volumes. We explored the relevance of these loci in two samples (Mental Illness Research Education and Clinical Centre [MIRECC] and Grady; n = 290) of trauma-exposed individuals enriched for PTSD and of diverse ancestry. Four of the previous loci demonstrated nominal evidence of replication in the MIRECC dataset, primarily within non-Hispanic whites (NHW). One locus replicated in the Grady cohort, which was composed exclusively of non-Hispanic blacks (NHB). Our data supported genetic interactions with diagnosis of lifetime PTSD and genetic interactions with childhood trauma in the MIRECC sample, but not the Grady sample. Given the racial, diagnostic, and trauma-exposure differences with the original genome-wide association study (GWAS) report, we conducted a full GWAS in the MIRECC and Grady datasets. Interactions between genetic variants and lifetime PTSD or childhood trauma were interrogated for single nucleotide polymorphisms (SNPs) with evidence of main effects. Genetic associations surpassed false discovery rate (FDR)-correction within hippocampal subfields in fimbria, subiculum, cornu ammonis-1 (CA1), and hippocampal amygdala transition area (HATA). One association was replicated in the Grady cohort (rs12880795 in TUNAR with left (L)-HATA volume). The most significant association in the MIRECC dataset was between rs6906714 in LINC02571 and right (R)-fimbria volume (p = 5.99×10−8, q = 0.0056). Interestingly, the effect of rs6906714 on R-fimbria volume increased with exposure to childhood trauma (gene*environment [G*E] interaction p = 0.022). These preliminary results argue for G*E interactions between genetic loci with PTSD and childhood trauma on hippocampal phenotypes. Our results underscore the need for larger neuroimaging-genetic studies in PTSD, trauma, and ancestrally diverse populations. [ABSTRACT FROM AUTHOR]

Intermittent fasting diet (IF) as a restrictive regimen prevents neural degeneration and stimulates overexpression of various neurotropic factors in the hippocampus of animal models. This study evaluates the potential effect of the IF in the prevention of learning and memory dysfunction and improving the alterations in the number and volume of neurons in an ethidium bromide (EB) induced mouse model of demyelination. Mice were randomly assigned into N group (Normal Diet and normal saline injection), F group (IF and normal saline injection), EBN group (Normal Diet and EB injection), EBF group (IF and EB injection). The hidden platform test was carried out based on path length, escape latency and swim speeds of mice. Stereological studies were determined by the Cavalieri and the Optical Dissector technique. Maintenance of mice on the IF results in significantly decreased the body weight and biochemical parameters, increased total number of neurons and volume of the hippocampus, and improved learning and memory parameters of adult male mice. However, IF in EBF group did not show as excellently as F group. The EBF group displayed significantly spatial memory improvement than that in EBN group. There were no statistically significant differences between EBF and EBN groups in stereological and learning parameters, though the EBF group displayed faster escape latencies, and swam faster and shorter path lengths than the EBN group in these parameters. Therefore as a conclusion, The IF fairly improved some adverse effects of EB in experimental demyelination models. [ABSTRACT FROM AUTHOR]

Objective: To emphasize the most appropriate magnetic resonance imaging (MRI) diffusion protocol for the detection of lesions that cause transient global amnesia, in order to perform an accurate examination, as well as to determine the ideal time point after the onset of symptoms to perform the examination. Materials and Methods: We evaluated five patients with a diagnosis of transient global amnesia treated between 2012 and 2015. We analyzed demographic characteristics, clinical data, symptom onset, diffusion techniques, and radiological findings. Examination techniques included a standard diffusion sequence (b value = 1000 s/mm2; slice thickness = 5 mm) and a optimized diffusion sequence (b value = 2000 s/mm2; slice thickness = 3 mm). Results: Brain MRI was performed at 24 h or 36 h after symptom onset, except in one patient, in whom it was performed at 12 h after (at which point no changes were seen) and repeated at 36 h after symptom onset (at which point it showed alterations in the right hippocampus). The standard and optimized diffusion sequences were both able to demonstrate focal changes in the hippocampi in all of the patients but one, in whom the changes were demonstrated only in the optimized sequence. Conclusion: MRI can confirm a clinical hypothesis of transient global amnesia. Knowledge of the optimal diffusion parameters and the ideal timing of diffusion-weighted imaging (> 24 h after symptom onset) are essential to improving diagnostic efficiency. [ABSTRACT FROM AUTHOR]

Antidepressants use during pregnancy was associated with an increased risk of autism spectrum disorders. Animal models based on early life alterations in serotonin availability replicate some of the anatomical and behavioral abnormalities observed in autistic individuals. In recent years there has been a growing interest in the possible role of the hippocampus in autism. The aim of study is to examine the effects of neonatal antidepressant (CTM) exposure during a sensitive period of brain development on pyramidal and granule cells density of hippocampal formation. We examined the pyramidal and granular cells density of dorsal hippocampus using Nissl stained sections obtained from neonatal citalopram (CTM) exposed rats (5 mg/kg, twice daily, s.c.), from postnatal day 8 to 21 (PN8-21), saline and non-exposed rats. The density of pyramidal cells was significantly increased by 10.2 % in CA1, 10.6 % in CA3 and 13.2 % in CA4 in CTM treated compared with non-treated or saline treated animals (p<0.0001). The density of granule cells in the dentate gyrus was significantly increased by 12.0 % in CTM treated compared with non-treated or saline treated animals (p<0.0001). These findings were obtained only from male rats, suggesting a sexual dimorphism in neural development after SSRI exposure. These data suggest that the neonatal exposure to CTM may induce long-lasting changes in the hippcampal formation in adults, and such effects appear to preferentially target males. [ABSTRACT FROM AUTHOR]

Objective: to identify whether maternal separation during breastfeeding (MSDB) affects the cellular count in different rat brain areas. The continuous mother-child interaction, adjusts and modulates the offspring behavioral response to environmental stimuli and also affects their development and homeostasis. Morphological and physiological changes in the offspring brains have been observed, including cell count changes in different brain areas with differences between males and females. Materials and methods: this study compared albino Wistar rats in a protocol of MSDB with a control group. Brain tissue was fixed with paraformaldehyde, cut in cryostat and either stained with Hematoxylin-Eosin (H&E) or processed for immunohistochemistry against glial fibrillary acidic protein (GFAP). All sections were analyzed using a cell count protocol including statistical analysis with Students T test at a significance level of P ≤0.05. Results: the MSDB group of male subjects presented higher GFAP-marked cell count in primary motor cortex and hippocampus; while female subjects, showed less GFAP-marked cell count in these same areas. Conclusions: MSDB produces sex-specific changes in the number of glial cells especially in the primary motor cortex, this finding may be considered as associated factor of alterations in motor responses to stress in these subjects, in addition to other known causes such as the Hypothalamic-Pituitary-Adrenal Axis dysfunction. [ABSTRACT FROM AUTHOR]

Unbalanced nutrition during perinatal period causes varying degrees of perturbations in the metabolism and cognitive functions of offspring. The aim of this study was to investigate effects of maternal and postweaning high-fat diet (HFD) exposure on the growth parameters, hippocampal functions and morphology of offspring in a sex-dependent manner. Spraque-Dawley rats were fed either standard (10 % fat) or saturated-fat (65 % fat) diet during their gestation and lactation period. After weaning, pups were sustained in same diet for 6 more weeks. Body mass index (BMI) of pups were monitored weekly, then spontaneous locomotor activities were recorded. Spatial learning and memory functions were analyzed by Morris Water Maze (MWM) test. Total volumetric changes of hippocampal subfields were estimated by Cavalieri method. HFD exposure produced sex-dependent alterations in BMI, serum lipid and activity levels. MWM results showed no significant difference among groups. However, retrieval indexes were higher in HFD-fed males. Total volumetric analysis of the dentate gyrus was comparable, but the pyramidal cell layer volume of HFD-fed males was lower than those of SD-fed males. Despite alterations in some growth and lipid parameters, maternal and perinatal exposure to HFD did not markedly affect cognitive functions and hippocampal morphology of offspring. [ABSTRACT FROM AUTHOR]

This investigation was undertaken in order to know whether the postnatal tactile/kinesthetic stimulation is effective in reversing the Prenatal Stress, in the cytoarchitecture of the CA3 region of the hippocampus, in female pups. 12 pups of female rats from the Sprague-Dawley strain were distributed to Control Group (GC), the Prenatal Maternal Stress by restriction group (EP) and Prenatal Maternal Stress with postnatal tactile/ kinesthetic stimulation Group (EP-ETK). The Prenatal Maternal Stress in female pups increased neuronal density in CA3b and CA3c areas (p<0.001). When compared to Prenatal Maternal Stress, pups prenatal stress who received early tactile/kinesthetic stimulation showed a decrease in neuronal density in CA3b and CA3c areas (p < 0,001). Postnatal tactile/kinesthetic stimulation was shown to successfully reverse the Prenatal Maternal Stress effects by decreasing neuronal density in CA3b and CA3c hippocampal areas. [ABSTRACT FROM AUTHOR]

Background: Childhood maltreatment is associated with alterations in morphology of stress susceptible brain regions. Maltreatment is also known to markedly increase risk for psychopathology and to have an enduring disruptive effect on sleep. Objective: To determine whether abnormalities in sleep continuity have effects on brain morphometry and to evaluate the extent to which sleep impairments mediate the effects of maltreatment on brain structure. Method: Maltreatment and Abuse Chronology of Exposure (MACE) scale ratings, actigraph-assessed sleep and 3T MRI were obtained on N = 37 18–19-year-old participants recruited from the community (N = 34 with neuroimaging). Results: Fourteen participants had no history of maltreatment while N = 23 were exposed, on average, to 4.7 types of maltreatment. Multiplicity of maltreatment was strongly associated with reduced sleep efficiency, increased wake after sleep onset time and number/duration of awakenings, which were independent of effects of maltreatment on depression and anxiety. The most important predictors of impaired sleep were exposure to parental non-verbal emotional abuse at 9–10 years of age. Reduced sleep efficiency correlated with reduced grey matter volume in hippocampus including CA1 subfield, molecular layer and dentate gyrus as well as inferior frontal gyrus and insula. Sleep mediated 39–46% of the effects of maltreatment on volume of hippocampal structures and inferior frontal gyrus. Conclusions: Actigraph-assessed sleep is disrupted in maltreated late teens and mediates a significant portion of the effects of maltreatment on hippocampal volume. Studies are needed to assess whether efforts to enhance sleep in maltreated children can pre-empt or ameliorate neurobiological consequences of maltreatment. [ABSTRACT FROM AUTHOR]

Introduction: The rationale of mesenchymal stem cells (MSCs) as a novel therapeutic approach in certain neurodegenerative diseases is based on their ability to promote neurogenesis. Hippocampal atrophy has been related to bipolar disorder (BD) in preclinical, imaging and postmortem studies. Therefore, the development of new strategies to stimulate the neurogenesis process in BD is crucial. Objectives: To investigate the behavioral and neurochemical changes induced by transplantation of MSCs in a model of mania-like behavior induced by lisdexamfetamine dimesylate (LDX). Methods: Wistar rats (n=65) received one oral daily dose of LDX (10 mg/kg) or saline for 14 days. On the 8th day of treatment, the animals additionally received intrahippocampal saline or MSC (1 µL containing 25,000 cells) or lithium (47.5 mg/kg) as an internal experimental control. Two hours after the last administration, behavioral and neurochemical analyses were performed. Results: LDX-treated rats had increased locomotor activity compared to saline-saline rats (p=0.004), and lithium reversed LDX-related hyperactive behavior (p<0.001). In contrast, the administration of MSCs did not change hyperlocomotion, indicating no effects of this treatment on LDX-treated rats (p=0.979). We did not find differences between groups in BDNF levels (p>0.05) in the hippocampus of rats. Conclusion: Even though these results suggest that a single intrahippocampal injection of MSCs was not helpful to treat hyperactivity induced by LDX and neither influenced BDNF secretion, we cannot rule out the possible therapeutic effects of MSCs. Further research is required to determine direct effects of LDX on brain structures as well as in other pathophysiological targets related to BD. [ABSTRACT FROM AUTHOR]

The present study describes the pharmacological analysis of the effects of carbachol, a cholinergic agonist, on hippocampal theta activity. Knowing that this activity is critically related to cognitive function and altered in patients with neurodegeneration, pharmacological efforts aiming to directly modulate hippocampal theta activity becomes of central importance. In a recently developed complete septo-hippocampal preparation, carbachol elicited significant theta power enhancement with 1 μM. Concentrations under 1 μM and over 2 μM carbachol caused significant reduction in the power of hippocampal theta activity. Carbachol effects were completely blocked with the cholinergic antagonist scopolamine. At the experimental level, it is the first time the direct action of a cholinergic agonist is evaluated in the septo-hippocampal pathway completely isolated. However, carbachol as a cholinergic agonist is a drug with a certain level of nonspecific response. That is why to correct this experimental limitation, we used scopolamine (cholinergic antagonist) which allowed us to corroborate the effects on the cholinergic pathway. In summary, electrophysiological assays demonstrated an effective concentration range of carbachol specifically modulating hippocampal theta activity. [ABSTRACT FROM AUTHOR]

Gestational diabetes mellitus (GDM) defined as impaired glucose tolerance affects approximately 6 % of all pregnant women who have never before had diabetes, but who do have high blood glucose levels during pregnancy. This study was done to evaluate the apoptosis in the neuronal cells in the CA1, CA2 and CA3 subfields of hippocampus and dentate gyrus in offspring of gestational diabetes at the 7, 21 and 28 d in postnatal rats. Thirty Wistar rat dams were randomly allocated in control and diabetic group. Dams in diabetic group were received 40 mg/kg/BW of streptozotocin at the first day of gestation and control groups received an equivalent volume normal saline injection intraperitoneally (IP). Six offspring of GDM and control dams, at the 7, 21, 28 postnatal day were randomly were sacrificed quickly with anesthesia. The coronal sections of brain serially collected. The apoptosis neurons were evaluated with TUNEL Assay. In the CA1, the number of apoptotic cells in 7, 21 and 28 d of postnatal life were significantly increased in GDM compared to controls (P<0.001). In the CA2, CA3 the number of apoptotic cells in 7, 21 and 28 d age-old offspring were significantly increased in GDM compared to controls (P<0.001). In the dentate gyrus, the number of apoptotic cells in 7, 21 and 28 d of postnatal life were significantly increased in GDM compared to controls (P<0.01). This study showed that the uncontrolled gestational diabetes significantly increases neuronal apoptosis in hippocampal and dentate gyrus in rat offspring. [ABSTRACT FROM AUTHOR]

Spirituality is the neurobiological basis for religion, and religion is the local interpretation of our spiritual feelings. Spiritual experiences can be visualized as brain activity. It is not proof for or against the existence of God. A number of neurobiological substrates play a role in «normal» religious experiences and in the mechanisms that cause neurological and psychiatric syndromes to be accompanied by changes in pathological religious experiences. Becoming a religious person or not is not a matter of free choice. The serotonergic system is thought to be an important biological basis for spiritual experiences. Polymorphisms in genes seem to determine our degree of spirituality. The often deeply religious/cosmic peak experiences that patients with temporal lobe epilepsy go through, due to, for instance, a tumor or to mesial/hippocampal sclerosis, is where, intriguingly, religion and neuroscience meet. As examples of this condition and the Gastaut-Geschwind syndrome symptoms, the apostle Paul, Muhammad, Joan of Arc, Vincent Van Gogh and Dostoyevsky are described. A convincing effect of praying for others has never been shown, yet the majority of people believe in the effectiveness of prayer. [ABSTRACT FROM AUTHOR]

The analysis of behaviors related to the conditioned fear is a central element in most studies of aversive classical conditioning, thus allowing the study of the processes of learning and aversive memory. Some studies highlight an important functional role of the hippocampus in the acquisition of the conditioned response in situations of conditioned fear. The learning situation of aversive classical conditioning is assessed by freezing behavior, concerning to the sound as well as to the context of the conditioning, and it is also evaluated by the magnitude of the response to the sound conditioned to an aversive stimulus. Studies on aversive classical conditioning are generally referred as fear conditioning based on the fact that the freezing behavior is part of the defense repertoire of rodents and other animals. The conditioning context is associated with brain structures that are not necessarily involved in the conditioning of a discrete an innocuous stimulus and an aversive stimulus, for example, sound-conditioning shock. The objective of this paper is to analyze the role of the hippocampus on aversive classical conditioning. The method used was a systematic review of the literature. Books and articles published in Pubmed, Science Direct and SciELO data in English and Portuguese languages were used. As a result, 38 papers were selected. We conclude that several studies have confirmed the important role of the hippocampus during acquisition and retrieval of aversive memory. In addition, the material presented here can be used to stimulate future research on the topic, fundamental point for the evolution of knowledge. [ABSTRACT FROM AUTHOR]

Hypoxia-ischemia (HI) is a major cause of brain damage in the newborn. Several studies elicited the neuroprotective effects of progesterone in adult rats but there is very little literature available on neonatal rats. Therefore the present study is undertaken to see the effect of progesterone in hypoxic ischemic brain injury in neonatal rats, using an established neonatal HI rat pup model. Sevenday- old rat pups were subjected to right common carotid artery ligation and then 60 minutes hypoxia. The first dose of progesterone to treatment group was administered by peritoneal injection (4 mg/kg), after 10 minutes of exposure and subsequent doses were given by subcutaneous injection at 6 h, 24 h and 48 h intervals. Control group was also exposed to HI and was given only the vehicle (peanut oil) through the same route and intervals as that of treatment group. After 96 h, the pups were perfused with 10% formalin and brains were sampled and stained with toluidine blue. Cells density and number of pyramidal cells of the hippocampal Cornu Ammonis (CA) regions were examined by stereological methods. The histomorphometric assessment of the effects of progesterone showed minimal but no significant protective value in the volume, cells density and total number of pyramidal cells of hippocampal CA region of the treatment and control groups (p>0.05) after HI. Our results concluded that 4 mg/kg of PROG had no significant neuroprotective effect in HI model of the neonatal rat's hippocampus. [ABSTRACT FROM AUTHOR]

Objective: although n-3 polyunsaturated fatty acids (PUFAs) play crucial roles in brain development and function, neither the optimal level of n-3 PUFAs nor the optimal ratio of n-6/n-3 PUFAs in the maternal diet are well defined. In this study, we investigated the effects of dietary n-6/n-3 PUFA ratios during pregnancy on neurogenesis and apoptosis in the brains of mouse offspring. Metods: female C57BL/6J mice were fed one of three diets with high, medium and low ratios of n-6/n-3 PUFAs (15.7:1, 6.3:1, 1.6:1), as well as a high fish oil diet with a n-6/n-3 ratio of 1:5.7; an n-3 PUFA-deficient diet served as control. The feeding regimens began two months before mouse conception and continued for the duration of the pregnancy. The neurogenesis and apoptosis of hippocampal CA3 area in the offspring were detected.Results: compared to the n-3 PUFA-deficient diet, n-3 PUFA-containing diets, particularly those with n-6/n-3 PUFA ratios of 6.3:1 and 1.6:1, significantly increased both phosphorylation of histone H3 at ser 10 (p-H3ser10) and calretinin-positive cells in hippocampus CA3 of the offspring. Furthermore, increased expression of Bcl2 protein, decreased expression of Bax protein, and reduced caspase 3 activity and numbers of TUNEL apoptotic cells were found in the three diets with high, medium and low n-6/n-3 PUFA ratios. However, there were no differences in any of these parameters between the high fish oil diet group and the n-3 PUFA-deficient diet group.Conclusions: these data suggest that a higher intake of n-3 PUFAs with a lower ratio of n-6/n-3 PUFAs of between about 6:1 to 1:1, supplied to mothers during pregnancy, may benefit brain neurogenesis and apoptosis in offspring. However, excessive maternal intake of n-3 PUFAs may exert a negative influence on brain development in the offspring. [ABSTRACT FROM AUTHOR]

This article reviews the role of the hippocampus in memory processing and its deterioration during aging in humans and animals, where even the neurochemical mechanisms underlying the decline in mnemonic ability are in process of understanding. Some aspects of the physiology of hippocampal will be developed, the type of memory depending on the hippocampal function will be discussed, and the molecular pathways that regulate memory function will be studied. Finally, it will be discuss the involvement of these mechanisms in the deterioration that occurs with this cognitive function during aging. It is concluded that the evidence suggests that deregulation of several signaling pathways, among which plays a central role the brain-derived neurotrophic factor, explains, ultimately, deterioration of memory in senescent organisms. [ABSTRACT FROM AUTHOR]

The hippocampus is a structure located in the depths of the temporal lobe, extending the full length of the floor of the anterior horn of the lateral ventricle. This structure is involved in learning, memory, emotional behavior, and motor control, making it a focus of great interest. Hippocampal volumetry is an imaging method used to determine the volume of the hippocampus, to support diagnosis of certain disorders. The hippocampus can be segmented in several ways, ranging from manual to fully automated methods; however, the manual method remains the reference standard. There are several manual segmentation protocols, and efforts are being made to establish an international consensus on standardization of this method. The hippocampal volume is obtained using the three viewing planes of T1 weighted images in volumetric sequences. Hippocampal volume is an aid in diagnosis of epilepsy of the temporal lobe, Alzheimer's disease, and mild amnesic cognitive disorder, among other conditions. [ABSTRACT FROM AUTHOR]

Ecstasy is one of the most popular amusing drugs among young people. Documents indicate some effects of Ecstasy on hippocampus and close relations between dopaminergic functions with reward learning. Therefore, the aim of this study was evaluation of the chronic effects of Ecstasy on memory in male Wistar rats and determination of dopamine receptors' gene expression in hippocampus. Forty adult male Wistar rats randomly distributed in five groups: Control, sham (received 1 ml/kg 0.9% saline) and three experimental groups were: Exp. 1 (2.5 mg/kg), Exp. 2 (5 mg/kg), and Exp. 3 (10 mg/kg) received MDMA intraperitoneally once every 7 days (3 times a day, 3 hours apart) for 4 weeks. Before the first injection animals trained in Shuttle Box memory and tested after the last injection. 24 hours after the final testing, brains of rats were dissected and hippocampus was removed and homogenized. After total RNA extraction and cDNA synthesis, expression of dopamine receptor genes in the hippocampus determined with Real-Time PCR. Our results showed that 2.5 and 5 mg/kg MDMA-treated groups had memory impairment. Also we found that MDMA increased the mRNA expression of dopamine receptors in hippocampus and the highest increase found in dopamine D1 receptors in the 5 mg/kg experimental group. We concluded that low doses of Ecstasy could increase Dopamine takers gene expression in hippocampus and disorder avoidance memory. But in high doses the increase in Dopamine takers gene expression was not as much as that in low doses and avoidance memory disorder was not observed. [ABSTRACT FROM AUTHOR]

Introduction. There are tools to quantitatively study the volume of the hippocampus. Such study would help to complement, more objectively and precisely, structural alterations that may be associated with the data obtained from electroencephalograms. Material and methods. Seventeen patients, between 3 and 11 years of age, with diagnosis of first-time seizures and from whom magnetic resonance studies and electroencephalograms were available, were analyzed. Results:.The left temporal lobe was involved in 3 patients, of whom 1 (5%) was found to be normal in the magnetic resonance and 2 (11%) abnormal with diagnoses of venous angioma and cortical atrophy. No significant difference was found between the two groups for the results obtained with resonance (Student p value: 0.6) and those obtained with electroencephalography (Student p value: 0.3). Electroencephalographic alterations in the frontal region were observed in 8 (47%) patients, 4 (23%) predominantly left, 1 (5%) right, and 3 (17%) bilateral; of those, in 5 (29%) cases the resonance was normal, one had left temporal atrophy, one diagnosis of meningitis, and one more of medulloblastoma. Discussion. In the remaining 3 (17%) patients we found generalized cortical involvement in the electroencephalogram, but resonance found one normal study, one suprasellar ependymoma, and one patient with agenesis of the corpus callosum. Conclusion. it was not possible to show a statistically significant value that could relate the results obtained by magnetic resonance with those obtained by electroencephalography. [ABSTRACT FROM AUTHOR]

Cholinergic system in CNS is involved in learning and memory. Scopolamine as muscarinic acetylcholine receptor antagonist is used for creation of memory impairment. The purpose of this study is evaluation of scopolamine-based amnesia on memory retention and the effect of this phenomenon on the number of neurons contains M1-receptors in the male Wistar rats hippocampal regions. Thirty-five male Wistar rats (200+20 g) were distributed randomly into five groups. Control group (intact samples) and 3 experimental groups with sham group (saline) were tested by the method of passive avoidance (shuttle box) in doses of 0.2, 0.5 and 1 mg/kg (intraperitoneally) as a single dose. After one week, memory test was taken from the rats. Finally, brains dissected from sacrificed rats, and then processed tissues were stained with antibody against M1 receptors (Immunohistochemistry technique) followed by counting of hippocampal CA1, CA3 and DG regions. Our results showed significant decrease in neurons contains M1-receptors in all area of hippocampus. We found that the less number of M1-neurons showed in 1 mg/kg dose of scopolamine. We concluded that scopolamine as muscarinic acetylcholine receptor antagonist can reduce dose-dependently the density of M1-neurons in all areas of hippocampus. [ABSTRACT FROM AUTHOR]

The capability to perceive and emit alarm substances, such as 2-hep-tanone, makes animals aware of the presence of danger, leading to some strategies directed towards survival. Strategies of survival involve emotional memory which is processed by deep temporal lobe structures, such as amygdaloid complex and hippocampus. In the Wi-star rat, 2-heptanone produces anxiety-like behavior and an increased firing rate of basal amygdaline neurons. However, it is unknown whether 2-heptanone modifies the responsivity of medial amygdaline-hippocampal connection. Therefore, we placed a group (n=10) of Wistar rats in a plexiglass cage impregnated with 2-heptanone. Rats from control group (n=10) were introduced into a similar clean cage. Twenty four hours later we obtained single-unit extracellular recordings from the hippocampus (CA1-CA3) neurons identified by their connection to medial amygdala. Although the basal neuronal firing rate was similar between groups, first order interval distribution histogram analysis showed that 2-heptanone produced shorter intervals of firing rate. Peristimulus histograms indicated that: i) the amygdaline stimulation produces an increased firing rate in hippocampal neurons; and ii) this response is increased and enlarged on the 2-heptanone group. Since a single exposure to an alarm pheromone seems to facilitate the amygdala-hippocampal connection, results suggest the initial formation of contextual memories related with fear. [ABSTRACT FROM AUTHOR]

Objective: To verify if the medicinal plants Panax ginseng C.A. Mey, Turnera diffusa Willd. ex Schult., and Heteropterys tomentosa O. Mach., which are amply used by the population as tonics and cognition enhancers, could have a protective effect on cell death by apoptosis, since this could be one of the mechanisms of action of these substances. Methods: Aged male Wistar rats (n=24) were divided into four groups. Over 30 days, three groups received treatments with hydroalcoholic extracts of the plants, and one group received saline solution. A fifth group with young adult male Wistar rats (n=4) received saline solution during the same period. Using the TUNEL technique, the percentage of apoptosis in the hippocampus of these animals was evaluated. Results: No differences were observed between the percentage of apoptotic cells in the hippocampus of aged animals and of young control animals. The percentage of apoptosis in the hippocampus of aged animals treated chronically with the extracts from the three plants also did not differ from the percentage of apoptosis in the hippocampus of the control group of aged animals. Conclusion: Treatment with the hydroalcoholic extracts of Panax ginseng, Turnera diffusa, and Heteropterys tomentosa did not influence the apoptosis of the hippocampal cells of aged rats. [ABSTRACT FROM AUTHOR]

Mental time travel includes the ability to bring to mind past events (episodic memory) and imagine future ones. Theory of mind is the ability to understand what others are thinking or feeling. Together, these faculties are dependent on the so-called “default mode network" in the brain, which is active when the mind is not engaged in interaction with the immediate environment. They enable us to mentally escape the present, and wander into past and future and into the minds of others. Language evolved out of gestural systems, probably during the Pleistocene, to enable people to share their mind wanderings, and tell stories, including fictional ones. [ABSTRACT FROM AUTHOR]

TRH expression and release from hypothalamic paraventricular nucleus (PVN) change with environmental stimuli. Fasted and food-restricted animals present decreased TRH synthesis and release, decelerating metabolic rate and utilization of energy stores, which is an advantageous adaptation of animals with nutrient deficit. Comparing thyroid axis function between prepuberal vs. adult male fasted animals, we found a greater body weight reduction than in adults (30% vs. 11%) and TRH release was not decreased; TRH degradation by pituitary PPII enzyme decreased, which maintained energy waste. TRH content of fasted-prepuberal animals changed in hippocampus and nucleus accumbens, and in amygdala of adults vs. ad libitum fed animals. PVN TRH role in food-avoiding behavior was studied by comparing its expression levels and of adolescent, adult females and male animals with anorexic conduct when drinking 2.5% of NaCl solution (AN) vs. a group forced to ingest the amount of food consumed by AN (FFR); also vs. a control group fed ad libitum (C). PVN TRH mRNA and TSH serum levels increased in AN vs. C; both decreased in FFR, supporting the putative anorexigenic role for the peptide. TRH content differentially changed in hippocampus and in frontal cortex of AN and FFR, suggesting its participation in taste perception and memory association. Orexinergic and NPYergic pathways are inactive in anorexic animals. Blocking corticotrophin-releasing hormone signal by an antagonist of CRH-R2 in the PVN reverses TRH high expression and TSH serum levels in AN. [ABSTRACT FROM AUTHOR]

As neuron-astrocyte interactions play a crucial role in the adult brain, it is thought that astrocytes support learning and memory through specific mechanisms. In this study, the effect of scopolamine based amnesia on the number of astrocytes in rats' hippocampus was studied. Adult male albino Wistar rats were bilaterally cannulated into the CA1 region and animals received saline or different doses of scopolamine (0.5,1 and 2 mg/ rat, intra - CA1), immediately after training. Then all the rats were sacrificed and coronal sections were taken from the dorsal hippocampal formation of the right cerebral hemispheres and stained with PTAH. The area densities of the astrocytes in dentate gyrus were measured and compared in the all groups (p < 0.05). Data showed that post-training scopolamine (0.5,1 and 2 mg/rat, intra-CA1) dose-dependently reduced the step-through latency in the inhibitory avoidance task, showing scopolamine-induced amnesia. Also we found different response of astrocytes in different subfields of hippocampal formation. In dentate gyrus the number of astrocytes was increased, but in other areas scopolamine can decreased the density of astrocytes. We concluded that scopolamine can cause amnesia and this phenomenon can have an effect on astrocyte numbers in the rats hippocampal formation. [ABSTRACT FROM AUTHOR]

Magnetic resonance images are useful in the study of experimental models of temporal lobe epilepsy. The manganese-enhanced MRI (MEMRI) technique is of interest since it combines the effects caused by manganese on the increased contrast in activated cell populations, when competing with calcium in synaptic transmission. Thus, the purpose of this study was to investigate the temporal evolution of the contrast related to manganese in the acute phase of temporal lobe epilepsy induced by systemic pilocarpine and compare it to the expression of the c-Fos protein. During this phase, the intensity of the MEMRI signal was analyzed at three different time points (5, 15 or 30 minutes) after the onset of status epilepticus (SE). The group that was maintained in status epilepticus for 30 minutes showed a decrease in intensity of the signal in CA1 and the dentate gyrus (DG). There were no differences between the control group and the other groups treated with pilocarpine. The expression of the protein, c-Fos, in the same animals showed that even in the short-duration status epilepticus (5 minutes), there was already maximal cellular activation in subregions of the hippocampus (DG, CA1 and CA3). Under the experimental conditions tested, our data suggest that the MEMRI signal was not sensitive for the identification of detectable variations of cell activation in the acute phase of the pilocarpine model. Our findings are not consistent with the idea that manganese contrast reflects primarily alterations in cellular activity during SE when other signal-modifying elements can act. [ABSTRACT FROM AUTHOR]

Objective: The hippocampus has an important role in the acquisition and recall of aversive memories. The objective of this study was to investigate the relationship among hippocampal rhythms. Methods: Microeletrodes arrays were implanted in the hippocampus of Wistar rats. The animals were trained and tested in a contextual fear conditioning task. The training consisted in applying shocks in the legs. The memory test was performed 1 day (recent memory) or 18 days (remote memory) after training. We proposed a measure based on the FFT power spectrum, denominated "delta-theta ratio", to characterize the different behaviors (active exploration and freezing) and the memories types. Results: The delta-theta ratio was able to distinguish recent and remote memories. In this study, the ratio for the 18-day group was smaller than for the 1-day group. Moreover, this measure was useful to distinguish the different behavior states - active exploration and freezing. Conclusions: The results suggest delta-theta oscillations could reflect the demands on information processing during recent and remote memory recalls. [ABSTRACT FROM AUTHOR]

Radiation therapy of the brain is associated with many consequences, including cognitive disorders. Pathogenesis of radiation induced cognitive disorder is not clear, but reduction of neurogenesis in hippocampus may be an underlying reason. 24 adult male rats entered to study. Radiation absorbed dose to midbrain was 10 Gy, delivered by routine cobalt radiotherapy machine which its output was measured 115.24 cGy/min. The rats were divided in four groups of sixes, including groups of control, single fraction 10 Gy, fractionated 10 Gy and finally anaesthesia sham group. Number of pyramidal nerve cells was counted in two regions of hippocampus formation (CA1 and CA3). The radiation could reduce the number of cells in two regions of hippocampus significantly (p=0.000). It seems fractionated 10 Gy irradiation to more efficient than single fraction, while role of anaesthesia drug should be cautiously assessed. Moreover the rate of neurogenesis reduction was determined the same in these regions of hippocampus meaning the same radiosensitivity of cells. [ABSTRACT FROM AUTHOR]

Methylazoxymethanol (MAM) and the non-protein amino acid ß-N-methyl-amino-L-alanine (L-BMAA) are neurotoxins contained in cycads. The consumption of cycads seeds produces locomotor impairment and rotational behavior in rats in the forced swim test. The present study investigated the neuroanatomical basis of these impairments. Thirty-two male Wistar rats were randomly divided into four groups: vehicle (1.0?l physiological saline), MAM (10nM), glutamate (10nM) and glutamate- MAM (10nM each). The treatments were microinjected every 24h for 7 days. The behavioral effects were evaluated in the forced swim and open field tests. Results: The vehicle did not modify locomotor activity in the open field test or produce rotational behavior in the forced swim test. Methylazoxymethanol promoted rotational behavior on the first day of treatment an effect that significantly decreased throughout the treatment, and increased sink time. Glutamate gradually increased rotational behavior throughout the treatment and the glutamate-MAM combination produced the greatest number of rotations, which significantly increased throughout the treatment. The MAM, glutamate and glutamate-MAM groups exhibited a significant decrease in the number of neurons in the CA1 and CA3 of the hippocampus compared with vehicle. Conclusion: The hippocampus participates in the expression of the locomotor impairment in rats in the forced swim test, an effect possibly mediated by excitatory effects at the neuronal level. [ABSTRACT FROM AUTHOR]

During the last decade neuroscientists have shown an increasing interest in adult neurogenesis and a number of studies have been focused on the role that it could play in learning and memory processes. Objective: the present work reviews the last evidences related to the possible role of adult neurogenesis in the hippocampus for learning and memory mechanisms. Development: one of the brain structures that generates new neurons during adulthood is the dentate gyrus of the Hippocampus. This structure is involved in learning and memory processes, and a plausible role for these newly born cells at the information processing level has been suggested. Conclusions: actual evidences do not provide a clear picture on the type of cognitive processes supported by adult-born neurons. Thus, different results have been found depending on the specific experimental and behavioural procedures used. Therefore, future research should consider how different tasks and experimental protocols affect to adult hippocampal neurogenesis in relationship to learning and memory mechanisms. [ABSTRACT FROM AUTHOR]

M-type potassium channel: channelopathie and role in epileptogenesis. Progress in the study of ion channels has made it possible to analyze the effects of human neurological disease-causing channel mutations at the level of the single channel, the subcellular domain, the neuronal network, and the behaving organism. Improper voltage-gated ion channels integration could cause several types of epilepsy. Neuronal KCNQ channels, voltage-dependent potassium channels that activate slowly but show no inactivation, correspond to the M channels that exert crucial influence over neuronal excitability. This review covers recent studies of the M-current (IM) and its participation over epileptogenesis. M-channels are now known to be composed of subunits of the Kv7 (KCNQ) K+ channel family. In humans, mutations in the Kv7.2 (KCNQ2) or Kv7.3 (KCNQ3) potassium-channel genes are associated with a form of juvenile epilepsy called benign familial neonatal convulsions (BNFC). Transgenic mice that conditionally express dominant-negative KCNQ2 subunits in brain, are associated with spontaneous seizures, behavioral hyperactivity and morphological changes in the hippocampus. It has been recently recognized that channelopathies can also include aberrant ion channel function that is acquired after an insult or injury to the brain. These acquired alterations are being investigated in animal models of temporal lobe epilepsy, where studies have shown functional changes in voltage-gated ion channels that lead to increases in excitability. These excitability changes could be related with IM inhibition. Therefore, epileptic hippocampal neurons may have altered the IM regulation. [ABSTRACT FROM AUTHOR]

The present study was planned to demonstrate the detailed immunoreactive (IR) distribution pattern of estrogen receptors (ER) in hippocampus of 15 female rats, adult, female Wistar rats in estrous phase. 30 μ m thick setions of hippocampal region fixed (4% buffered paraformaldehyde) were obtained with cryostat. The sections were processed free- floating for immunolocalization of ER using, mouse monoclonal anti-ER-α antibody with PAP technique. The results showed presence of ER immunoreactive neurons in all the subfields of hippocampus with some variations. In cornua ammonis (CA) maximum ER positive (+ve) neurons were localized in CA3 region. Layer analysis showed maximum localization in the stratum oriens (SO) region. In other subfields and layers of CA the IR neurons were comparatively less in number. The morphological characters of all ER +ve neurons showed them to be interneurons both in CA as well as in Dentate gyrus (DG). [ABSTRACT FROM AUTHOR]

Approximately, half of the patients with progressive sepsis develop encephalopathy, but there is scarce knowledge onto question that how the sepsis associated encephalopathy contributes brain dysfunction. Hippocampus is one of the most vulnerable regions during experimental sepsis. In the present study, effects of sepsis on the neuronal density and morphology in CA1, CA3 and DG areas were investigated in a rat model of intraperitoneal sepsis. Twenty-four Wistar rats were divided into three different groups: faecal peritonitis group, sham-operated and un-operated control groups. Pyramidal neuron volume density was significantly higher in CA1 area of the faecal peritonitis group compared to both un-operated (p<0.05) and sham-operated (p<0.05) groups. Pyramidal neuron volume density was also significantly higher in CA3 area of the faecal peritonitis group compared to both un-operated (p<0.05) and shamoperated (p<0.05) groups. Mean nuclear diameter of pyramidal neurons in CA1 area of the faecal peritonitis group was significantly lower (p<0.05) compared to un-operated control group. Dark, shrunken neurons were frequently observed and neuroglial cells appeared to be prevalent in the faecal peritonitis group compared to control groups. These results collectively suggest that intraperitoneal sepsis does not initiate cell death in the early stages of sepsis, although morphological signs of neurodegeneration start to appear. [ABSTRACT FROM AUTHOR]

The pyramidal cell density of CA1 hippocampal subfield following STZ-induced diabetes in young rats were studied. 12 male albino 6-week Wistar rats were allocated equally in groups of normal and diabetic. Hyperglycemia induced by Streptozotocin (80 mg/kg) in animals of diabetic group. After 5 weeks of study, all the rats were sacrificed and coronal sections were taken from dorsal hippocampal formation of the right cerebral hemispheres and stained with crysel violet. The area densities of the CA1 pyramidal cells were measured and compared among two groups. No significant difference between the densities of two experimental groups was found. The results can arise from the short period of diabetes and also the possible regenerative processes in developing brain of the young diabetic rats which compensated significant diabetes-induced neuronal loss. [ABSTRACT FROM AUTHOR]

Up to the moment five proteins are known, structurally related that constitute the neurotrophin family that belong to brain derived neurotrophic factor (BDNF) that has influence on many types of neurons in the central nervous system, promoting neuronal differentiation, growth, and survival. This protein is important in the neuroprotection, as well as in the mechanisms of synaptic plasticity. In this work we evaluate the BDNF contents in cerebral tissue from normal rats due to the importance of this factor in neuroplasticity phenomena, and the lack of normative data in the literature regarding the normal values of this protein in hippocampus, cortex, and striatum. Wistar male rats weighing from 200 to 250 g were used as experimental animals (n = 20). The samples were homogenized, and the BDNF concentration was measured using an immunoenzymatic system. There were no significant differences in the BDNF concentrations between homologous areas in both cerebral hemispheres right and left for the studied homologous areas, although a tendency to the decrease was evidenced in the left side concerning the right side when was compared. The concentration in hippocampus was higher than the one detected in the striatum and cortex, while BDNF concentration in the striatum and cortex did not show significant differences among them. This work allowed the established reference values of BDNF , which will be very useful for the future studies that research on the potentialities and neuroplasticity mechanisms, in the normal nervous system, as well as the recovery of lost functions. [ABSTRACT FROM AUTHOR]

Learning and memory are neurobiological processes close related and necessary to have consciousness. The present review focuses on the neuroanatomy structures close related with the function of learning and memory. The interaction between different neuroanatomical structures and their repeated neurophysiological activity is integrated as an exclusive neural networks. In the cortex, these neural networks are different forms of learning and memory, which activity induced plastic changes in synaptic functions that lead to the strengthening of the synaptic connections with the result of reconstructed permanent traces that evoke memories. For instance a specific damage in hippocampus is manifested by recent memory disturbances or by the incapacity to acquire new knowledge. Other brain cortical or neocortical specific lesions, induces alterations particularly related with that cerebral region and to the integrative function level. This is, learning and memory are not confined to a single place in the brain. During the course of our lives we learn a lot of things. Nevertheless, learning and memory could be affected at any time. Further basic research is needed in order to get a better understanding about the physiology and anatomical structures involved in memory and learning. [ABSTRACT FROM AUTHOR]

In this study we aimed to investigate the effects of intrahippocampal injection of scopolamine (an antagonist of M1 muscarinic receptors with amnesic effects) on the behavior of rats evaluated on elevated plus-maze. The animals were tested in the plus-maze immediately after the drug injection and re-tested after 24 h without the drug effect. We analyzed the open and closed arms exploration in each session, and also the behavioral profile in each session using the minute by minute analyses. The results showed increases in the open arms exploration to the scopolamine animals in the first session. The minute by minute analyses in this session showed a maintenance of the exploration during the session, conversely to the observed in the saline animals when in the third minute is showed a significant reduction in comparison to the first minute. These results show that the scopolamine leads to impair the mechanism of acquisition and consolidation of the information during the session, without altering the long term memory processes. [ABSTRACT FROM AUTHOR]

Humans organize past events as "memories", i.e. what we learn is encoded and stored in the brain, and by accumulating relevant environmental information we better cope with similar situations in the future. The main research on memory began in the 70s and the most important conclusions have been derived, on the one hand, from animal experiments, and on the other hand, from clinical studies of amnesic patients. Many classification systems of memory have been proposed. First, authors have distinguished among the different phases involved in the process of memory formation: short-term and long-term memory. Second, declarative and non-declarative memories have been recognized. Last, researchers have conceived the need to evaluate memory in a systematic manner through behavioral as well as pharmacological means, in different moments or times to be able to have independent access to the study of the different memory phases or types of memory. This approach to the study of memory has allowed evaluating drug effects on memory and also understanding the molecular mechanisms involved in memory processes. In addition, this research has also aimed at studying brain regions implicated in the diverse memory phenomena under investigation. [ABSTRACT FROM AUTHOR]