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Two specimens of Pacific Seahorse, Hippocampus ingens Girard, 1858, were captured as a bycatch in trawl fishing off the Chañaral coast, in the Atacama region of northern Chile. This finding expands its known distribution area in Chilean coastal territory by 114 km to the south, highlighting the importance of documenting its geographical range and the need for further research and sampling to gain a better understanding of the population in the area.

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]

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Introdução: Estudos mostram que o exercício físico tem a capacidade de influenciar o sistema nervoso central, de forma a trazer benefícios à saúde humana através do estímulo da neurogênese, sinaptogênese e angiogênese cerebral. O hipocampo é tido como uma região do sistema nervoso central com elevada plasticidade, mediante, principalmente, à neurogênese. Esta, por sua vez, pode ser influenciada de forma negativa por fatores como o envelhecimento e estresse, e positivamente por estímulos como o reforço cognitivo e o exercício físico. Ressaltando a importância da neuroplasticidade hipocampal, principalmente na vida adulta, bem como a influência que o ambiente exerce nesse processo. Objetivo: Realizar uma revisão integrativa a respeito da plasticidade hipocampal induzida pelo exercício físico. Matérias e Métodos: Foram reunidos artigos científicos publicados nas bases de dados da Biblioteca Virtual em Saúde e PUBMED do ano 2018 até março de 2023, com os descritores: neuronal plasticity AND exercise, incluindo seus termos relacionados em português. Resultados: Diversos estudos apresentam o exercício físico como uma ótima ferramenta de prevenção e tratamento adjuvante para inúmeras condições patológicas. Conclusão: Os artigos selecionados corroboram com o resultado de que o exercício físico tem impacto positivo na neuroplasticidade hipocampal. Sendo as atividades aeróbicas de moderada a alta intensidade, atividade resistida leve/moderada e treinamento motor-espacial, os exercícios com maior impacto cerebral

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]

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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]

BackgroundChildhood 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.ObjectiveIn 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.MethodIn 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.ResultsVolume 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).ConclusionsCT 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.

Introducción: en pacientes con epilepsia del lóbulo temporal refractarios que no son candidatos a cirugía, se debe considerar la estimulación eléctrica cerebral como una opción. Contenido: la estimulación eléctrica cerebral es la administración directa de pulsos eléctricos al tejido nervioso que permite modular un sustrato patológico, interrumpir la manifestación clínica de las crisis y reducir la gravedad de estas. Así, dada la importancia de estos tratamientos para los pacientes con epilepsia del lóbulo temporal refractaria, se hace una revisión de cuatro tipos de estimulación eléctrica. La primera, la del nervio vago, es una buena opción en crisis focales y crisis generalizadas o multifocales. La segunda, la del hipocampo, es más útil en pacientes no candidatos a lobectomía por riesgo de pérdida de memoria, con resonancia magnética normal o sin esclerosis mesial temporal. La tercera, la del núcleo anterior, es pertinente principalmente en pacientes con crisis focales, pero debe realizarse con precaución en pacientes con alto riesgo de cambios cognitivos, como los ancianos, o en los que presentan alteración del estado de ánimo basal, y, por último, la del núcleo centromediano se recomienda para el tratamiento crisis focales en el síndrome de Rasmussen y crisis tónico-clónicas en el síndrome de Lennox-Gastaut. Conclusiones: el interés por la estimulación eléctrica cerebral ha venido aumentando, al igual que las estructuras diana en las cuales se puede aplicar, debido a que es un tratamiento seguro y eficaz en pacientes con epilepsia del lóbulo temporal para controlar las crisis, pues disminuye la morbimortalidad y aumenta la calidad de vida.

Copyright of Acta Neurológica Colombiana is the property of Colombian Association of Neurology / Asociacion Colombiana de Neurologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Acta Neurológica Colombiana is the property of Colombian Association of Neurology / Asociacion Colombiana de Neurologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction: Worldwide, approximately 50 million people have dementia, with Alzheimer disease (AD) being the most common type, accounting for 60%-70% of cases. Given its high incidence, it is imperative to design studies to expand our knowledge about its onset and development, and to develop early diagnosis strategies and/or possible treatments. One methodological strategy is the use of transgenic mouse models for the study of the factors involved in AD aetiology, which include oxidative stress and the immune response. Development: We searched the PubMed, Scopus, and Google Scholar databases for original articles and reviews published between 2013 and 2019. In this review, we address 2 factors that have been studied independently, oxidative stress and the immune response, in transgenic models of AD, and discuss the relationship between these factors and their impact on the loss of synaptic and structural plasticity, resulting in cognitive impairment. Conclusion: This review describes possible mechanisms by which oxidative stress and the immune response participate in the molecular, cellular, and behavioural effects of AD, observing a close relationship between these factors, which lead to cognitive impairment. Resumen: Introducción: En el mundo, alrededor de 50 millones de personas padecen demencia; la forma más común es la enfermedad de Alzheimer (EA), que representa el 60–70% de los casos. Dada su alta incidencia, se hace imperativo diseñar estudios que permitan ampliar el conocimiento sobre su aparición y desarrollo, para proponer diagnósticos tempranos y/o posibles tratamientos. Una de las estrategias metodológicas que se han desarrollado son los modelos transgénicos murinos para el estudio de los factores involucrados en su etiología, y entre ellos, el estrés oxidativo y la respuesta inmune. Desarrollo: Se realizó una búsqueda de artículos originales y revisiones en PubMed, Scopus y Google Scholar (2013–2019). En esta revisión abordamos dos factores que han sido estudiados de forma independiente: el estrés oxidativo y la respuesta inmune en modelos transgénicos para la EA, y se discute la relación que existe entre ellos y que impacta en la pérdida de la plasticidad sináptica y estructural, produciendo como efecto final el deterioro cognitivo. Conclusión: Esta revisión describe posibles mecanismos en donde participan el estrés oxidativo y la respuesta inmune sobre los efectos moleculares, celulares y conductuales en la EA, observando una estrecha relación entre estos elementos que conducen hacia el deterioro cognitivo.

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Introducción: con la experiencia de los registros electroencefalográficos invasivos y el fracaso quirúrgico después de la cirugía, se ha hecho evidente que la epilepsia del lóbulo temporal es mucho más compleja de lo que se creía, y en la actualidad es considerada una enfermedad de redes anatomofuncionales y no de lesiones estructurales. Contenido: la información neurofisiológica e imagenológica actual permite concluir que en esta epilepsia están involucradas varias redes neuronales temporales y extratemporales que contribuyen a la extensión de la zona epileptógena. Una forma de entender el concepto de red epiléptica en la epilepsia del lóbulo temporal es a partir del conocimiento de la corteza piriforme. Varios estudios clínicos han mostrado que en pacientes con epilepsia del lóbulo temporal asociada a esclerosis hipocampal existe una disfunción interictal del procesamiento olfatorio que es más significativa, en comparación con pacientes con epilepsia focal extrahipocampal y controles sanos. Esta alteración es, probablemente, la consecuencia de una red neuronal disfuncional que se extiende más allá del hipocampo y que afecta a otras estructuras cercanas, incluida la corteza piriforme. Conclusión: en este artículo llevamos a cabo una revisión narrativa de la literatura con el objetivo de establecer un vínculo entre la corteza piriforme y la epileptogénesis del lóbulo temporal, y demostramos que esta enfermedad es la consecuencia de una disfunción de redes neuronales que no depende exclusivamente de una anormalidad estructural en el hipocampo o en estructuras cercanas.

Introducción. Las lesiones del nervio facial afectan la plasticidad a largo plazo en el hipocampo, así como la memoria de reconocimiento de objetos y la memoria espacial, dos procesos dependientes de esta estructura. Objetivo. Caracterizar en ratas el efecto de la lesión unilateral del nervio facial sobre la activación de células de la microglía en el hipocampo contralateral. Materiales y métodos. Se hicieron experimentos de inmunohistoquímica para detectar células de la microglía en el hipocampo de ratas sometidas a lesión irreversible del nervio facial. Los animales se sacrificaron en distintos momentos después de la lesión, para evaluar la evolución de la proliferación (densidad de células) y la activación (área celular) de la microglía en el tejido del hipocampo. Los tejidos cerebrales de los animales de control se compararon con los de animales lesionados sacrificados en los días 1, 3, 7, 21 y 35 después de la lesión. Resultados. Las células de la microglía en el hipocampo de animales con lesión del nervio facial mostraron signos de proliferación y activación a los 3, 7 y 21 días después de la lesión. Sin embargo, al cabo de cinco semanas, estas modificaciones se revirtieron, a pesar de que no hubo recuperación funcional de la parálisis facial. Conclusiones. La lesión irreversible del nervio facial produce proliferación y activación temprana y transitoria de las células de la microglía en el hipocampo. Estos cambios podrían estar asociados con las modificaciones electrofisiológicas y las alteraciones comportamentales dependientes del hipocampo descritas recientemente.

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Background: Hippocampal volume is recognised as a surrogate imaging biomarker for the study of Alzheimer's disease (AD). However, in Cuba there are no antecedents of its use. The objective of this research was to establish an automatic hippocampal segmentation procedure to study a sample of Cuban subjects diagnosed with possible mild or moderate AD. Methodology: A total of 104 subjects with mean ages of 73.77 ± 6.74 years participated. Imaging for the calculation of hippocampal volumes and asymmetry index (AI) was performed with a Siemens Magnetom Allegra 3T scanner using an MP-RAGE sequence. Volumes were obtained manually and automatically using Amira 5.3 and FreeSurfer 6.0 software, respectively. The results of both methods were statistically compared. Results: The steps for hippocampal volumetric quantification were established for these methods. Comparison between them showed high concordance (ICC = 0.95) for both hippocampi. Therefore, there were no significant differences between them. The mean right (2961.84 ± 552.70 mm3) and left (2892.68 ± 536.6 mm3) volumes of the subjects were obtained. These volumes and the asymmetry index were significantly different with respect to a sample of healthy subjects with (p = 0.00001) and (p = 0.003) respectively; and similar to those obtained in a sample of subjects with AD in Latin America. Conclusions: A procedure for automated volumetric quantification of the hippocampus was established. This allowed the study of a Cuban sample with possible AD. This constitutes a previous step to longitudinally evaluate the effectiveness of new Cuban drugs. Resumen: Introducción: El volumen del hipocampo es reconocido como un biomarcador imagenológico subrogado para el estudio de la Enfermedad de Alzheimer (EA). Sin embargo, en Cuba no hay antecedentes de su uso. El objetivo de esta investigación fue establecer un procedimiento de segmentación automática del hipocampo para estudiar una muestra de sujetos cubanos diagnósticados con posible EA leve o moderada. Métodos: Participaron 104 sujetos con edades promedio de 73.77 ± 6.74 años. Las imágenes utilizadas para el cálculo de los volúmenes hipocampales y el índice de asimetría (IA) se realizó con un escáner Siemens Magnetom Allegra 3T usando una secuencia MP-RAGE. La obtención de los volúmenes se hizo de forma manual y automática usando el programa Amira 5.3 y FreeSurfer 6.0 respectivamente. Se compararon estadísticamente los resultados de ambos métodos. Resultados: Se establecieron los pasos para la cuantificación volumétrica del hipocampo para estos métodos. La comparación entre ellos mostró alta concordancia (CCI = 0.95) para ambos hipocampos. Por tanto, no existieron diferencias significativas entre ellos. Se obtuvieron los volúmenes medios derecho (2961.84 ± 552.70 mm3) e izquierdo (2892.68 ± 536.6 mm3) de los sujetos. Estos volúmenes y el índice se asimetría fueron significativamente diferentes respecto una muestra de sujetos sanos con (p = 0.00001) y (p = 0.003) respectivamente; y similares a los obtenidos en una muestra de sujetos con EA en América Latina. Conclusiones: Quedó establecido un procedimiento para la cuantificación volumétrica automatizada del hipocampo. Esto permitió el estudio de una muestra cubana con posible EA. Constituyendo un paso previo para evaluar longitudinalmente la efectividad de nuevos medicamentos cubanos.

Introducción: El trastorno por estrés postraumático afectan la salud mental de los pacientes pediátricos, se considera muy común en estos pacientes. Estudios científicos apoyados en la resonancia magnética han fundamentado una estrecha relación entre el estrés postraumático y cambios estructurales en el cerebro. Se realizó una revisión bibliográfica en el periodo de abril a mayo de 2021, en los recursos disponibles en MEDLINE, SciELO, Pubmed y Elsevier. Del total de consultas se citaron 25 referencias. Objetivo: Describir los signos radiológicos en la neuroimagen de pacientes pediátricos con estrés postraumático. Desarrollo: Los estudios de neuroimagen en niños y adolescentes con trastorno por estrés postraumático se han centrado en estructuras anormales y la funcionalidad de algunas regiones individuales del cerebro; estas implican las regiones cerebrales asociadas con la fisiopatología, ellas son: la corteza prefrontal medial y dorsolateral; la corteza orbitofrontal; ínsula; núcleo lentiforme; amígdala; hipocampo y el parahipocampo; la corteza cingulada anterior y posterior; el precúneo; cúneo; el giro fusiforme y lingual y los tractos de materia blanca que conectan estas regiones cerebrales. Conclusiones: Los signos radiológicos en la neuroimagen de pacientes pediátricos con trastorno por estrés postraumático son: reducción de los volúmenes del hipocampo; del volumen cerebral e intracraneal y del volumen de la amígdala, así como una disminución del área total del cuerpo calloso. Además se observa que el volumen hipofisario y los volúmenes de materia gris cerebral fueron menores en los pacientes con estrés postraumático.

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]

Copyright of Brazilian Journal of Biology is the property of Instituto Internacional de Ecologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introducción: Recientemente hemos mostrado que la estimulación eléctrica de la amígdala 15 min después del entrenamiento de una tarea de memoria espacial puede facilitar el aprendizaje espacial en animales con lesión de fimbria-fórnix. Objetivos: estudiar los mecanismos de plasticidad neural involucrados en la recuperación funcional en los animales con lesión de fimbria-fórnix por efecto de la estimulación eléctrica de la amígdala basolateral. Métodos: Las proteínas y genes relacionados con la plasticidad neural se midieron en el hipocampo y la corteza prefrontal de ratas con lesión en la fimbria-fórnix después de cuatro días de entrenamiento en el laberinto acuático y estimulación de la amígdala basolateral. Resultados: La estimulación de la amígdala aumenta en el hipocampo los niveles de BDNF; así como los genes relacionados con la plasticidad neural bdnf y arc en los animales lesionados. Estas evidencias sugieren que estos pueden ser algunos de los mecanismos involucrados en la recuperación de las funciones perdidas en animales con lesión de fimbria-fórnix con estimulación de amígdala. Además, la estimulación de la amígdala aumenta la expresión transitoria de la proteína c-Fos; e incrementa las proteínas MAP-2 y GAP-43 que son indicadores del crecimiento dendrítico y axonal respectivamente en la corteza prefrontal y el hipocampo. Conclusiones: En consecuencia, la estimulación de la amígdala puede activar regiones cerebrales relevantes para los procesos de memoria y activar todas las formas de plasticidad neural, lo que lleva a la restauración neurológica.

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]

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]

Las lesiones cerebrales de cualquier etiología, incluyendo traumatismos, enfermedades neurodegenerativas o accidentes cerebrovasculares, suponen alteraciones irreversibles en la función cognitiva, el sistema motor y somato sensorial, e incluso de personalidad. En la actualidad no existen tratamientos eficientes, por tanto, la búsqueda de opciones terapéuticas para aumentar la tasa de reemplazo neuronal en el sistema nervioso central es uno de las líneas de investigación más activas en la neurociencia actual. En este sentido, el descubrimiento de la reposición neuronal a partir de células madre neurales (NSC) en el sistema nervioso central (SNC) adulto ha supuesto un nuevo enfoque en el desarrollo de terapias para este tipo de lesiones cerebrales. El descubrimiento de células madre neurales (NSC) en el cerebro adulto, abrió la posibilidad del desarrollo de nuevas terapias neurorregenerativas basadas en la reposición neuronal a partir de NSC (neurogénesis). En condiciones fisiológicas, existe neurogénesis a partir de NSC en dos zonas del cerebro adulto: el hipocampo y la zona subventricular (SVZ), mientras que en el resto del cerebro adulto no existe neurogenesis o es escasa. Sin embargo, cuando hay una lesión cerebral, estas NSC son reclutadas en el perímetro donde se produjo y se puede ver como proliferan células con características de precursores neurales (NPC). En esta publicación se hace una revisión exhaustiva de los conocimientos actuales sobre la neurogénesis en cerebro adulto.

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]

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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]

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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]

Copyright of Revista Brasileira de Anestesiologia is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)