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Microplastics (MPs) have emerged as widespread environmental pollutants, causing significant threats to aquatic ecosystems and organisms. This review examines the toxic effects of MPs on fishes, with a focus on neurobehavioural, physiological, and reproductive impacts, as well as the underlying mechanisms of toxicity. Evidence indicates that MPs induce a range of neurobehavioural abnormalities in fishes, affecting social interactions and cognitive functions. Altered neurotransmitter levels are identified as a key mechanism driving behavioural alterations following MP exposure. Physiological abnormalities in fishes exposed to MPs are also reported, including neurotoxicity, immunotoxicity, and oxidative stress. These physiological disruptions can compromise the individual health of aquatic organisms. Furthermore, reproductive abnormalities linked to MP exposure are discussed, with a particular emphasis on disruptions in endocrine signaling pathways. These disruptions can impair reproductive success in fish species, impacting population numbers. Here we explore the critical role of endocrine disruptions in mediating reproductive effects after exposure to MPs, focusing primarily on the hypothalamic-pituitary-gonadal axis. Our review highlights the urgent need for interdisciplinary research efforts aimed at elucidating the full extent of MP toxicity and its implications for aquatic ecosystems. Lastly, we identify knowledge gaps for future research, including investigations into the transgenerational impacts, if any, of MP exposure and quantifying synergetic/antagonistic effects of MPs with other environmental pollutants. This expanded knowledge regarding the potential risks of MPs to aquatic wildlife is expected to aid policymakers in developing mitigation strategies to protect aquatic species.

Mucopolysaccharidosis type IIIA (MPS IIIA) is an inherited metabolic disorder caused by a lysosomal enzyme deficiency resulting in heparan sulphate (HS) accumulation and manifests with a progressive neurodegenerative phenotype. A naturally occurring MPS IIIA mouse model is invaluable for preclinical evaluation of potential treatments but the ability to effectively assess neurological function has proved challenging. Here, the aim was to evaluate a set of behaviour tests for their reliability in assessing disease progression in the MPS IIIA mouse model. Compared to wild-type (WT) mice, MPS IIIA mice displayed memory and learning deficits in the water crossmaze from mid-stage disease and locomotor impairment in the hind-limb gait assessment at late-stage disease, supporting previous findings. Declined wellbeing was also observed in the MPS IIIA mice via burrowing and nest building evaluation at late-stage disease compared to WT mice, mirroring the progressive nature of neurological disease. Excessive HS accumulation observed in the MPS IIIA mouse brain from 1 month of age did not appear to manifest as abnormal behaviours until at least 6 months of age suggesting there may be a threshold of HS accumulation before measurable neurocognitive decline. Results obtained from the open field and three-chamber sociability test are inconsistent with previous studies and do not reflect MPS IIIA patient disease progression, suggesting these assessments are not reliable. In conclusion, water cross-maze, hind-limb gait, nest building and burrowing, are promising assessments in the MPS IIIA mouse model, which produce consistent results that mimic the human disease.

Gliclazide (GLD), a sulphonylurea is efficacious in the treatment of diabetes type-2. However, there is limited information on its activity in the brain, especially in diabetics. This research investigated the brain activities of GLD following streptozotocin-induced diabetes in Wistar rats. Twenty five adult male Wistar rats (200–250 g) were grouped (n = 5) as: Control (distilled water, 5 mL/kg) and GLD (150 mg/kg) groups; and the diabetic groups, untreated streptozotocin (STZ, 35 mg/kg), and STZ (35 mg/kg) treated with GLD (150 mg/kg) for two and four weeks, and already on high fat diet. The animals’ body weights and blood glucose levels were checked weekly. After the experimental duration, spontaneous alternation and novel object recognition tests were carried out and the animals sacrificed. Perfusion with phosphate buffered saline preceded brain excision for biochemical analyses, with halves fixed in 10% neutral buffered formalin for histology. Compared with the control, results showed (p

Environmental pollution and work related hazard have exposed humans to various metallic agents including, mercury. The protective effect of Allium sativum (A. sativum) Linn (Garlic) on mercury-induced oxidative stress in the cerebellum of adult female Wistar rats was studied. Twenty five adult female Wistar rats weighing between 180g and 210g, used for this study were divided into five groups; Group 1 rats received distilled water and served as the control, group 2 rats were administered 3.75mg/kg body weight of Mercury (II) chloride (Hgcl2) only, group 3 rats were administered 50mg/kg body weight of A. sativum extract only, group 4 rats were administered 3.75mg/kg Hgcl2 and 50mg/kg of A. sativum extract and group 5 were administered 3.75mg/kg Hgcl2 and 100mg/kg vitamin C orally for 28 days. The body weight and neurobehavioral studies were done shortly before sacrifice on day 29. After sacrifice, the brain was dissected out and the cerebellum, processed for biochemical and histolomorphological evaluations. Data were analyzed using ANOVA at p<0.05. Results showed signs of general body weakness, decline in food and water intake, and decreased weight gain in the Hgcl2 and A. sativum + Hgcl2 groups compared with the control and other treated groups. There was reduced drop-off time in the forelimb grip strength in the Hgcl2-treated groups compared with the control. An increased lipid peroxidation, and decreased glutathione levels, SOD and GPx activities was seen in the cerebellum of Hgcl2-treated group compared with the control and other treated groups. Histomorphologically, there was reduction in the molecular layer thickness, loss of Purkinje cells and increased astrocytes population in the cerebellum of the Hgcl2-treated group compared with the control and the other treated groups. In conclusion, exposure to mercury affected muscle tone, induced oxidative stress causing morphological alterations. Aqueous extracts of Allium sativum and vitamin C decreased the rate at which mercury induced oxidative damage in the cerebellum of adult female Wistar rats. [ABSTRACT FROM AUTHOR]

Microplastics (MPs) have emerged as widespread environmental pollutants, causing significant threats to aquatic ecosystems and organisms. This review examines the toxic effects of MPs on fishes, with a focus on neurobehavioural, physiological, and reproductive impacts, as well as the underlying mechanisms of toxicity. Evidence indicates that MPs induce a range of neurobehavioural abnormalities in fishes, affecting social interactions and cognitive functions. Altered neurotransmitter levels are identified as a key mechanism driving behavioural alterations following MP exposure. Physiological abnormalities in fishes exposed to MPs are also reported, including neurotoxicity, immunotoxicity, and oxidative stress. These physiological disruptions can compromise the individual health of aquatic organisms. Furthermore, reproductive abnormalities linked to MP exposure are discussed, with a particular emphasis on disruptions in endocrine signaling pathways. These disruptions can impair reproductive success in fish species, impacting population numbers. Here we explore the critical role of endocrine disruptions in mediating reproductive effects after exposure to MPs, focusing primarily on the hypothalamic-pituitary-gonadal axis. Our review highlights the urgent need for interdisciplinary research efforts aimed at elucidating the full extent of MP toxicity and its implications for aquatic ecosystems. Lastly, we identify knowledge gaps for future research, including investigations into the transgenerational impacts, if any, of MP exposure and quantifying synergetic/antagonistic effects of MPs with other environmental pollutants. This expanded knowledge regarding the potential risks of MPs to aquatic wildlife is expected to aid policymakers in developing mitigation strategies to protect aquatic species. • Fish exposed to MPs exhibit neurotoxicity, immunotoxicity, and oxidative stress. • MPs disrupt neurotransmitters in fish, affecting social interactions and cognitive function. • MP exposure disrupts fish hormonal signaling pathways, impacting reproductive function. [ABSTRACT FROM AUTHOR]

The objective designated to discover the analgesic effect of nefopam in the normal (non-stressed) chickens and its possible alteration due to hydrogen peroxide (H2O2)-induced oxidative stress (OS) in 7-14 day old chickens. The analgesia of nefopam has been increased by 47% in the stressed chickens by measuring the analgesic Median Effective Dose (ED50) value. This value was 9.10 mg/kg, IM in the normal chickens where it became 4.80 mg/kg, IM in stressed chickens. There is a significant rise in the antinociceptive action of nefopam 18 mg/kg, IM by 88% in the stressed group of chickens in comparison with the normal one elicited by an electro-stimulation and formaldehyde 0.05 ml of 0.1% tests for induction of nociception. The observations showed several significant stimulatory modifications in the neurobehaviour when nefopam treated with a subtle dosage 1 mg/kg, IM in the stressed chickens concerning the latency to move, squares crossed and time of the tonic immobility response test. Significant damage was detected in the liver function when nefopam injected at 18 mg/kg, IM in stress chickens in comparison to normal one by 28, 33 and 65% as estimated through Alkaline phosphatase (ALP), Aspartate trans-aminase (AST) and Alanine trans-aminase (ALT) concentrations in the serum, respectively. The sum of data findings indicated that H2O2-inducedOS increased the analgesic activity of nefopam in the chickens; despite the changes occur on the neurobehaviour and liver function. The dose of nefopam should be reduced when preparing the therapeutic regimen in the stressed animals.

Spirulina platensis is rich in nutritional profile and a great source of prebiotic with neuro-protective properties. Stress is an inevitable part of today's lives, affecting people differently, and individuals with resilient adaptations are less vulnerable to it. The present study aims at evaluating Spirulina as a prebiotic supplement in the early life of zebrafish to cope with chronic unpredictable stress (CUS) in its later stage of life. Zebrafish 5dpf larvae were fed with 1% Spirulina formulated diet for 90 days, and then adult zebrafish were subjected to CUS for 15 days to evaluate the diet's response to chronic stress. The observations were compared by studying the anxiety level through behavioural test, gut microbiota composition analysis, and the effect on the myelin sheath at the ultrastructural and molecular levels. In zebrafish given the Spirulina supplemented diet, CUS did not induce anxiety-like behaviour, Spirulina supplementation lowered the Firmicutes to Bacteroidetes ratio and helped in myelin protection, with a significant decrease in the myelin g-ratio and upregulation of myelin-related genes bdnf, mpz, olig2 and sox10 which resulted in mitigating the effect of stress as compared to fish fed with a normal diet. To conclude, Spirulina supplementation in the early life of zebrafish helps to reduce the effects of a chronic unpredictable stress. However, Spirulina's protective effect against overall stress needs to be evaluated further., Competing Interests: Declaration of competing interest The authors declare no conflict of interest., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Lead is a systemic toxicant that affects virtually every organ system, primarily the central nervous system, through an increase in the production of reactive oxygen species (ROS). This increase in ROS overwhelms the natural antioxidant system of the body leading to oxidative stress. Some plants such as Vernonia amygdalina have been reported to possess antioxidant activity which counteracts the damage induced by free radicals. Accordingly, this study was designed to investigate the possible protective activity of aqueous Vernonia amygdalina leaf extract against lead-induced neurotoxicity in adult Wistar rats. Thirty Wistar rats were randomised into six groups (A-F) consisting of five rats each for a study period of 28 days. Group A served as the control group, Group B was administered with 100mg/kg body weight of lead only, Groups C and D were pretreated with 200mg/kg and 400mg/kg bodyweight of aqueous Vernonia amygdalina leaf extract and 100mg/kg body weight of lead respectively. Groups E and F were administered with 200mg/kg and 400mg/kg body weight of aqueous Vernonia amygdalina leaf extract only. The Open field and Novel Object Recognition tests were assessed and thereafter, the cerebellum, cerebrum and hippocampus were harvested for histological examination. Results showed a significant decrease in the body and brain weights, ambulation, rearing and discrimination index as well as a conversely significant increase in grooming and immobility in lead-treated rats. Histological examination of lead-alone treated groups showed loss of some Purkinje cells in the cerebellum, degenerating pyramidal cells in the cerebrum and altered morphology with pyknotic nuclei in the hippocampus. Pretreatment of rats with Vernonia amygdalina attenuated lead-induced alterations to body and brain weights, neurobehavioural activities and tissue histomorphology, thus indicating a potent protective activity. These findings provide the first research evidence that Vernonia amygdalina protects against lead-induced neurotoxicity in Wistar rats. [ABSTRACT FROM AUTHOR]

Mercury (Hg) exposure is known to damage vital components of the central nervous system primarily through oxidative stress. Although Phyllanthus amarus (PA) is reported to be rich in antioxidants, there is a dearth of relevant research evidence to show its protective activity against Mercuric chloride (HgCl2)-induced neurotoxicity. Accordingly, this study was designed to investigate the possible protective activity of aqueous Phyllanthus amarus leaf extract (APALE) in HgCl2-exposed rats using standard neurobehavioral assessments. Thirty adult Wistar rats were randomized into six groups of five rats each viz: A: Control, distilled water; B: HgCl2 (4 mg/kg body wt.); C: APALE (200 mg/kg body wt.) + HgCl2 (4 mg/kg); D: APALE (400 mg/kg body wt.) + HgCl2 (4 mg/kg); E: APALE (200 mg/kg body wt.); F: APALE (400 mg/kg body wt.). All administrations were through an orogastric tube for 14 days. Thereafter, neurobehavioral tests (open field, novel object and Y-maze) were done and experimental rats were sacrificed by cervical dislocation. Body, brain and cerebellar weights were examined across all groups. HgCl2 exposure significantly (p<0.0.05) decreased whole body weight across experimental groups. Similarly, a reduction in brain and cerebellar weight was observed. Significant neurobehavioral alterations to locomotion, discrimination index and cognition/memory, induced by HgCl2, were observed across experimental groups. However, protection against the deleterious effects induced by HgCl2 was observed following pretreatment with APALE. Conclusively, these findings show that APALE demonstrated potent protective activity against HgCl2-induced neurotoxicity and may be useful in the management of Hg toxicity and other related disorders. [ABSTRACT FROM AUTHOR]

Mercury (Hg) exposure is known to damage vital components of the central nervous system primarily through oxidative stress. Although Phyllanthus amarus (PA) is reported to be rich in antioxidants, there is a dearth of relevant research evidence to show its protective activity against Mercuric chloride (HgCl2)-induced neurotoxicity. Accordingly, this study was designed to investigate the possible protective activity of aqueous Phyllanthus amarus leaf extract (APALE) in HgCl2-exposed rats using standard neurobehavioral assessments. Thirty adult Wistar rats were randomized into six groups of five rats each viz: A: Control, distilled water; B: HgCl2 (4 mg/kg body wt.); C: APALE (200 mg/kg body wt.) + HgCl2 (4 mg/kg); D: APALE (400 mg/kg body wt.) + HgCl2 (4 mg/kg); E: APALE (200 mg/kg body wt.); F: APALE (400 mg/kg body wt.). All administrations were through an orogastric tube for 14 days. Thereafter, neurobehavioral tests (open field, novel object and Y-maze) were done and experimental rats were sacrificed by cervical dislocation. Body, brain and cerebellar weights were examined across all groups. HgCl2 exposure significantly (p

Consumption of a high-fat diet has adverse impacts on metabolism, neurobehavioral, and neurochemical homeostasis in both humans and experimental animals. Here, we examined the effects of two different cultivars of Corylus avellana L. in a mouse model of metabolic syndrome. Corylus avellana L. reduced weight gain in mice that were treated with a high-fat diet, improved their behavioral parameters as exemplified by locomotion and rearing, working-memory, and reduced grooming and anxiety indices. Both Corylus avellana L. varieties reduced blood glucose levels and lipid peroxidation, improved lipid profile, and antioxidant status in mice placed on a high fat diet. Finally, brain acetylcholinesterase activity was also reduced, dopamine level was increased, while caspase-3 level was reduced. Thus, the Corylus avellana L. cultivars improve metabolic, behavioral, and neurochemical homeostasis in a diet with a high-fat content.

Caffeine is globally consumed as a stimulant in beverages. It is also ingested in purified forms as power and tablets. Concerns have been raised about the potential consequences of intrauterine and early life caffeine exposure on brain health. This study modeled caffeine exposure during pregnancy and early postanal life until puberty, and the potential consequences. Caffeine powder was dissolved in distilled water. Thirty-two (n = 32) pregnant mice (Mus musculus) (dams) were divided into four groups- A, B, C and D. Group A animals served as a control, receiving placebo. Caffeine doses in mg/kg body weight were administered as follows: Group B, 10 mg/kg; Group C, 50 mg/kg; Group D, 120 mg/kg. Prenatal caffeine exposure [phase I] lasted throughout pregnancy. Half the number of offspring (pups) were sacrificed at birth; the rest were recruited into phase II and the experiment continued till day 35, marking puberty. Brain samples were processed following sacrifice. γ-aminobutyric acid (GABA), acetylcholine (ACh), and serotonin (5Ht) neurotransmitters were assayed in homogenates to evaluate functional neurochemistry. Anxiety and memory as neurobehavioural attributes were observed using the elevated plus and Barnes' mazes respectively. Continuous caffeine exposure produced positive effects on short and long-term memory parameters; the pattern interestingly was irregular and appeared more effective with the lowest experimental dose. Anxiety test results showed no attributable significant aberrations. Caffeine exposure persistently altered the neurochemistry of selected neurotransmitters including ACh and 5Ht, including when exposure lasted only during pregnancy. ACh significantly increased in group BC+ to 0.3475μgg-1 relative to control's 0.2508μgg-1; pre-and continuous postnatal exposure in Group B increased 5Ht to 0.2203 μgg-1 and 0.2213 μgg-1 respectively relative to control's 0.1863 μgg-1. From the current investigation, caffeine exposure in pregnancy had persistent effects on brain functional attributes including neurotransmitters activities, memory and anxiety. Caffeine in moderate doses affected memory positively but produced negative effects at the higher dosage including increased anxiety tendencies. [ABSTRACT FROM AUTHOR]

Persons with certain single nucleotide polymorphisms (SNPs) in the CACNA1D gene (encoding voltage-gated calcium channel subunit alpha 1-D) have increased risk of developing neuropsychiatric disorders such as bipolar, schizophrenia and autism. The molecular consequences of SNPs on gene expression and protein function are not well understood. Thus, the use of animal models to determine genotype-phenotype correlations is critical to understanding disease pathogenesis. Here, we describe the behavioural changes in larval zebrafish carrying an essential splice site mutation (sa17298) in cacna1da. Heterozygous mutation resulted in 50% reduction of splice variants 201 and 202 (haploinsufficiency), while homozygosity increased transcript levels of variant 201 above wild type (WT; gain-of-function, GOF). Due to low homozygote viability, we focused primarily on performing the phenotypic analysis on heterozygotes. Indeed, cacna1dasa17298/WT larvae displayed hyperlocomotion—a behaviour characterised in zebrafish as a surrogate phenotype for epilepsy, anxiety or psychosis-like behaviour. Follow-up tests ruled out anxiety or seizures, however, as neither thigmotaxis defects nor epileptiform-like discharges in larval brains were observed. We therefore focused on testing for potential "psychosis-like" behaviour by assaying cacna1dasa17298/WT larval locomotor activity under constant light, during light-dark transition and in startle response to dark flashes. Furthermore, exposure of larvae to the antipsychotics, risperidone and haloperidol reversed cacna1da-induced hyperactivity to WT levels while valproate decreased but did not reverse hyperactivity. Together, these findings demonstrate that cacna1da haploinsufficiency induces behaviours in larval zebrafish analogous to those observed in rodent models of psychosis. Future studies on homozygous mutants will determine how cacna1d GOF alters behaviour in this context. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is a highly toxic heavy metal. It accumulates in biological tissues, especially in fish which constitutes a first rank food for humans, particularly in the coastal areas. This study investigates the effect of long-term exposure to low Cd concentration (17 μg/kg/day) in rat striatum and hippocampus. In this study, the neurobehavioral ability changes were assessed by applying cognitive standard testing at the end of the rats' exposure period. In addition, the examination of mitochondrial swelling was performed at the same time of evaluation of its redox status in the brain regions studied through stress parameters (GSH, MDA, GST, and CAT). This study examined also whether this long-term exposure can modify the apoptotic signaling pathway via assessment of apoptotic markers (caspase-8 and 9, Bax, Bcl-2, and Cyt-c) in cell lysates. The results of this study showed changes in neurobehavioral abilities of animals and a stronger mitochondrial swelling associated with a significant decrease in antioxidant systems (GSH, GST, and CAT) and conversely an increase in the lipoperoxidation end product (MDA) in both the striatal and hippocampal mitochondria. In addition, the results revealed a significant increase in pro-apoptotic intracellular components such as caspase-9, Cyt-c, and Bax, and showed also an evident decrease in Bcl-2 levels. In conclusion, our results reported that chronic exposure to Cd produces behavioral and cognitive perturbations, enhances oxidative stress associated with mitochondrial edema and Cyt-c leakage, and, ultimately, potentiates apoptosis signaling pathway in both brain regions in rats. [ABSTRACT FROM AUTHOR]

• Accumulations of manganese in the brain assessed with T1-weighted MRI. • No clear association between manganese exposure and fine motor functions. • Welders showed normal motor functions on the MDS-UPDRS part III scores. • Welders performed better on a steadiness test than controls. • Limitations: cross-sectional, newspaper recruitment, disparities in education. The aim of this study was to evaluate the effect of exposure to manganese (Mn) on fine motor functions. A total of 48 welders and 30 unexposed workers as controls completed questionnaires, underwent blood examinations, and a motor test battery. The shift exposure of welders to respirable Mn was measured with personal samplers. For all subjects accumulations of Mn in the brain were assessed with T1-weighted magnetic resonance imaging. Welders showed normal motor functions on the Movement Disorder Society-Sponsored Revision of the Unified Parkinson Disease Rating Scale part III. Furthermore welders performed excellent on a steadiness test, showing better results than controls. However, welders were slightly slower than controls in motor tests. There was no association between fine motor test results and the relaxation rates R1 in globus pallidus and substantia nigra as MRI-based biomarkers to quantify Mn deposition in the brain. [ABSTRACT FROM AUTHOR]

Background: This study explored the mechanisms underlying altered neurobehavioural development of female offspring born to mothers with polycystic ovary syndrome (PCOS). Methods: In total, 20 women with PCOS and 32 healthy women who underwent caesarean deliveries with a single female foetus were recruited. Infants were assessed with Dubowitz scoring. Swan71 cell line with stable FOS overexpression was used to verify the regulatory effects of FOS on brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) expression. Learning and memory in female first-generation (F1) and second-generation (F2) offspring in a rat model of PCOS was tested using the Morris water maze at puberty and adulthood. Transcriptome analysis of pubertal hippocampi and hypothalami of female F1 offspring was conducted. Findings: Total score and behaviour subscales of Dubowitz scoring were significantly lower in female infants of women with PCOS. FOS and NGF protein levels were downregulated in placental villi of the PCOS group. FOS played a key role in BDNF inhibition and enhancing NGF in Swan71 cells. PCOS female F1 rats exhibited lower target crossing times during puberty when compared to controls. Transcriptome analysis revealed significant changes in hippocampal and hypothalamic neuronal pathways in female F1 rats at puberty. Interpretation: FOS regulation of neurotrophins in the placenta negatively affects neurobehavioural development of female offspring of PCOS mothers. Funding: This study was funded by the National Key R&D Program of China (2018YFC1004900 to F.Q. and F.W.) and the National Natural Science Foundation of China (81874480 to F.Q.; 81873837 to F.W.).

Abstract Background Research on reproductive health effects on children from low-level, long-term exposure to pesticides currently used in the agricultural industry is limited and those on neurobehavioral effects have produced conflicting evidence. We aim at investigating the association between pesticide exposure on the reproductive health and neurobehavior of children in South Africa, by including potential relevant co-exposures from the use of electronic media and maternal alcohol consumption. Methods The design entails a prospective cohort study with a follow-up duration of 2 years starting in 2017, including 1000 school going children between the ages of 9 to 16 years old. Children are enrolled with equal distribution in sex and residence on farms and non-farms in three different agricultural areas (mainly apple, table grapes and wheat farming systems) in the Western Cape, South Africa. The neurobehavior primary health outcome of cognitive functioning was measured through the iPad-based CAmbridge Neuropsychological Test Automated Battery (CANTAB) including domains for attention, memory, and processing speed. The reproductive health outcomes include testicular size in boys and breast size in girls assessed in a physical examination, and blood samples to detect hormone levels and anthropometric measurements. Information on pesticide exposure, co-exposures and relevant confounders are obtained through structured questionnaire interviews with the children and their guardians. Environmental occurrence of pesticides will be determined while using a structured interview with farm owners and review of spraying records and collection of passive water and air samples in all three areas. Pesticide metabolites will be analysed in urine and hair samples collected from the study subjects every 4 months starting at baseline. Discussion The inclusion of three different agricultural areas will yield a wide range of pesticide exposure situations. The prospective longitudinal design is a further strength of this study to evaluate the reproductive and neurobehavioural effects of different pesticides on children. This research will inform relevant policies and regulatory bodies to improve the health, safety and learning environments for children and families in agricultural settings.

Introduction: Hydrocephalus is a disorder in which the circulation of cerebrospinal fluid is altered in a manner that leads to its accumulation in the ventricles and subarachnoid space. Its impact on the neuronal density and networks in the overlying cerebral cortex in a time-dependent neonatal hydrocephalic process is largely unknown. We hypothesize that hydrocephalus will affect the cytoarchitecture of the cerebral cortical mantle of neonatal hydrocephalic mice, which will in turn modify sensorimotor processing and neurobehaviour. Objective: The purpose of this study is to probe the effect of hydrocephalus on 3 developmental milestones (surface righting reflex, cliff avoidance reflex, and negative geotaxis) and on cortical neuronal densities in neonatal hydrocephalic mice. Methods: Hydrocephalus was induced in 1-day-old mice by intracisternal injection of sterile kaolin suspension. The pups were tested for reflex development and sensorimotor ability using surface righting reflex (PND 5, 7, and 9), cliff avoidance (PND 6), and negative geotaxis (PND 10 and 12) prior to their sacrifice on PND 7, 14, and 21. Neuronal density and cortical thickness in the sensorimotor cortex were evaluated using atlas-based segmentation of the neocortex and boundary definition in 4-μm paraffin-embedded histological sections with hematoxylin and eosin as well as cresyl violet stains. Results: Surface righting and cliff avoidance activities were significantly impaired in hydrocephalic pups but no statistically significant difference was observed in negative geotaxis in both experimental and control pups. The neuronal density of the sensorimotor cortex was significantly higher in hydrocephalic mice than in age-matched controls on PND 14 and 21 (373.20 ± 21.54 × 10−6 μm2 vs. 157.70 ± 21.88 × 10−6 μm2; 230.0 ± 44.1 × 10−6 μm2 vs. 129.60 ± 3.72 × 10−6 μm2, respectively; p < 0.05). This was accompanied by reduction in the cortical thickness (µm) in the hydrocephalic mice on PND 7 (2,409 ± 43.37 vs. 3,752 ± 65.74, p < 0.05), PND 14 (2,035 ± 322.10 vs. 4,273 ± 67.26, p < 0.05), and PND 21 (1,676 ± 33.90 vs. 4,945 ± 81.79, p < 0.05) compared to controls. Conclusion: In this murine model of neonatal hydrocephalus, the quantitative changes in the cortical neuronal population may play a role in the observed changes in neurobehavioural findings. [ABSTRACT FROM AUTHOR]

Aim: Prenatal exposure to cigarettes leads to alterations in brain development during pregnancy. This has an impact on postnatal psychological and behavioural processes, affecting an infant's neurobehavioural profile with little known about which aspects are affected. The evidence was synthesised to assess the effects of prenatal cigarette smoke exposure on neurobehavioural outcomes within the first year of life.Methods: Six databases were searched (Web of Science Core Collections, MEDLINE, PsycINFO, CINAHL, EBSCOhost eBook Collection and OpenGrey) in November 2018. Eligible studies (n = 17) had to include a measure of prenatal cigarette exposure and a neurobehavioural assessment ≤1 year of age.Results: In the first year of life, specific areas of neurobehavioural functioning are related to prenatal cigarette exposure with eight out of 10 areas of neurobehaviour having significant medium (negative affect, attention, excitability, irritability and orientation) or small (muscle tone, regulation and difficult temperament) pooled effect sizes. Only lethargy and stress did not show any significant pooled effects.Conclusion: Prenatal cigarette exposure affects a significant range of behaviours during the first year of life. [ABSTRACT FROM AUTHOR]

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In this study, the persistent effects of embryonic exposure to fenbuconazole (FBZ), a triazole fungicide, on neurobehaviour in zebrafish were investigated. After exposure of fertilized eggs to FBZ for 72 h (h), the larvae were cultured to adulthood in clean water. In adult zebrafish embryonically exposed to 50 and 500 ng L−1 FBZ, the ratio of brain weight/body weight was significantly decreased, and the number of apoptotic cells in the brain was significantly increased, accompanied by upregulated protein levels of P53 and downregulated levels of BCL2. The novel tank test showed a significant reduction in the moved distance and speed, and a longer period of adaptation to new environments in the 500 ng L−1 group. The social preference experiment showed impaired social interaction behaviour and reduced time of aggregation in the 500 ng L−1 group. Increased dopamine and norepinephrine levels in the brain might be responsible for this anxiety-like behaviour. In addition to upregulated protein levels of tyrosine hydroxylase and β 2 -adrenoceptor, the transcription of genes related to dopamine and norepinephrine synthesis in the brain such as th1 , th2 , ddc , drd1b , dat , and dbh, was increased. The methylation levels of related genes were reduced, which were matched with their increased transcriptional levels. These results demonstrate that embryonic FBZ exposure might cause persistent neurotoxicity in adulthood, which suggests the rational cautious use of FBZ. [Display omitted] • Embryonic exposure to FBZ caused impairments on neurobehavior in adult zebrafish. • FBZ reduced the brain/body index and increased number of apoptotic cells in the adult brain. • The synthesis of dopamine (DA) and norepinephrine (NE) in the adult brain was enhanced. • Reduced methylation levels of related genes matched with their increased transcription. [ABSTRACT FROM AUTHOR]

The rapid modulation of chromatin organization is thought to play a crucial role in cognitive processes such as memory consolidation. This is supported in part by the dysregulation of many chromatin-remodelling proteins in neurodevelopmental and psychiatric disorders. A key example is ATRX, an X-linked gene commonly mutated in individuals with syndromic and nonsyndromic intellectual disability. The consequences of Atrx inactivation for learning and memory have been difficult to evaluate because of the early lethality of hemizygous-null animals. In this study, we evaluated the outcome of brain-specific Atrx deletion in heterozygous female mice. These mice exhibit a mosaic pattern of ATRX protein expression in the central nervous system attributable to the location of the gene on the X chromosome. Although the hemizygous male mice die soon after birth, heterozygous females survive to adulthood. Body growth is stunted in these animals, and they have low circulating concentrations of insulin growth factor 1. In addition, they are impaired in spatial, contextual fear and novel object recognition memory. Our findings demonstrate that mosaic loss of ATRX expression in the central nervous system leads to endocrine defects and decreased body size and has a negative impact on learning and memory.

• Methylparaben altered hatching and heart rate. • Methylparaben altered anxiety-like and exploratory behaviour. • Methylparaben dose-dependently increased cortisol levels. • Methylparaben decreased AChE activity in exposed larvae. Parabens are widely used as antimicrobial preservatives. Recent studies have reported the endocrine disrupting effects of these chemicals, especially methylparaben. Previously, we have reported the alteration in Vtg gene expression upon exposure to environmentally relevant doses of methylparaben in zebrafish (Danio rerio) embryos. However, studies reporting neurobehavioural outcomes on exposure to methylparaben are limited. Therefore, this study was aimed at investigating the methylparaben-induced effects on developmental and neurobehavioural endpoints. Zebrafish embryos were exposed to sub-lethal concentrations of methylparaben: 0.1 ppb, 1 ppb, 10 ppb and 100 ppb. Alterations in developmental landmarks such as heart rate and hatching percentage were observed in embryos exposed to 10 ppb and 100 ppb of methylparaben. Results obtained from the novel tank diving test established that anxiety-like behaviour is induced in larvae exposed to 0.1 ppb and 1 ppb of methylparaben. A significant inhibition in the acetylcholinesterase (AChE) activity was also recorded in methylparaben-exposed groups. An increase in cortisol levels was observed in the exposed groups, which further supports the observations made in the novel tank diving test, establishing methylparaben as an anxiogenic agent even at sub-lethal concentrations. The underlying molecular mechanism needs further elucidation to investigate whether the behavioural effects are proximally or distally induced by early developmental exposure to methylparaben. [ABSTRACT FROM AUTHOR]

Iron oxide (Fe2O3) nanoparticles (NPs) attract the attention of clinicians for its unique magnetic and paramagnetic properties, which are exclusively used in neurodiagnostics and therapeutics among the other biomedical applications. Despite numerous research findings has already proved neurotoxicity of Fe2O3-NPs, factors affecting neurobehaviour has not been elucidated. In this study, mice were exposed to Fe2O3-NPs (25 and 50 mg/kg body weight) by oral intubation daily for 30 days. It was observed that Fe2O3-NPs remarkably impair motor coordination and memory. In the treated brain regions, mitochondrial damage, depleted energy level and decreased ATPase (Mg2+, Ca2+ and Na+/K+) activities were observed. Disturbed ion homeostasis and axonal demyelination in the treated brain regions contributes to poor motor coordination. Increased intracellular calcium ([Ca2+]i) and decreased expression of growth associated protein 43 (GAP43) impairs vesicular exocytosis could result in insufficient signal between neurons. In addition, levels of dopamine (DA), norepinephrine (NE) and epinephrine (EP) were found to be altered in the subjected brain regions in correspondence to the expression of monoamine oxidases (MAO). Along with all these factors, over expression of glial fibrillary acidic protein (GFAP) confirms the neuronal damage, suggesting the evidences for behavioural changes. [ABSTRACT FROM AUTHOR]

With increasing evidence of neurodevelopmental problems faced by late preterm children, there is a need to explore possible underlying brain structural changes. The use of brain magnetic resonance imaging has provided insights of smaller and less mature brains in infants born late preterm, associated with developmental delay at 2 years. Another useful tool in the newborn period is neurobehavioural assessment, which has also been shown to be suboptimal in late preterm infants compared with tern infants. Suboptimal neurobehaviour is also associated with poorer 2-year neurodevelopment in late preterm infants. More research into these tools will provide a better understanding of the underlying processes of developmental deficits of late preterm children. The value of their role in clinical care remains to be determined. [ABSTRACT FROM AUTHOR]

The effect of P-alaxin on some neurobehavioural parameters was studied in Swiss white mice. 21 mice were randomly assigned to three groups (n=7) namely; control group, clinical dose group and high dose group. Animals in control group received normal rat chow and standard feed ad libitum. Animals in the clinical dose group were given P-alaxin at a dose of 0.01mg/kg body weight while animals in the high dose group were given P-alaxin at a dose of 0.02mg/kg body weight. The results obtained showed that, in the open field maze test, the clinical dose and high dose groups showed significant increase (P<0.05) in stretch attend posture compared to control. Conversely, there was a significant decrease (P<0.05) in line crossings of high and clinical dose groups when compared to control. In the light/dark transition box test, the clinical and high dose groups showed a significant decrease (P<0.05) in the frequency of line crossings when compared to control. In the morris water maze test, the high and clinical dose groups showed a significant inncrease in frequency of swimming latency when compared to control group. From the total analysis obtained, P-alaxin decreases locomotion and exploratory activities, it impairs motivation and the tendency to investigate the environment as well as reduction in visuospartial learning and memory. [ABSTRACT FROM AUTHOR]

Cyclophosphamide use has been associated with increased oxidative stress in cells and tissues. Quercetin's antioxidative properties make it of potential benefit in such conditions of oxidative stress. To assess quercetin's ability to mitigate cyclophosphamide–induced organ toxicities in rats. Sixty rats were assigned into six groups. Groups A and D served as normal and cyclophosphamide control and were fed standard rat chow, groups B and E were fed quercetin supplemented diet (100 mg/kg of feed), while those in groups C and F were fed quercetin at 200 mg/kg of feed. Groups A-C received intraperitoneal (ip) normal saline on days 1 and 2, while D-F received ip cyclophosphamide (150 mg/kg/day on days 1 and 2). On day 21, behavioural tests were carried out, animals were sacrificed and blood samples taken. Organs were processed for histological study. Quercetin reversed cyclophosphamide-induced decrease in body weight, food intake and total antioxidant capacity, and increase in lipid peroxidation (p = 0.001), It also reversed derangement in levels of liver transaminase, urea, creatinine and proinflammatory cytokines (p = 0.001). Improvement in working-memory and anxiety-related behaviours were also observed. Finally, quercetin reversed alterations in levels of acetylcholine, dopamine and brain-derived neurotropic factor (p = 0.021); while reducing serotonin levels and astrocyte immunoreactivity. Quercetin shows significant ability to protect against cyclophosphamide-induced changes in rats. [ABSTRACT FROM AUTHOR]

Background and Objectives: There are scarce data on post-stroke neurobehavioral disability (NBD). The aim of this study was to identify the prevalence of NBD in a subacute inpatient stroke population and examine potential associations with demographic, stroke-related, functional and psychosocial variables. Methods: 82 survivors of stroke were consecutively recruited during their inpatient rehabilitation admission. Nursing staff rated NBD in patients using the St Andrews -Swansea Neurobehavioral Outcome Scale (SASNOS). Measures of patient functional independence (FIM), cognition (MoCA), and mood symptoms (HADS) were collected in addition to nursing reports of whether observed NBD negatively impacted on the patient or those around them. Results: NBD relating to interpersonal relationships (44.4% of participants) and cognition (52.4%) were highly prevalent within the sample while NBD relating to inhibition (1.2%), aggression (3.6%), and communication (2.5%) were relatively rare. Presence of NBD was significantly associated with reduced functional independence (rs=0.39, p < 0.01) and associated with trends in cognitive impairment (rs=0.29, p = 0.03), increased anxiety (rs=-0.43, p = 0.02) and depressive symptoms (rs=-0.43, p = 0.02). Presence of NBD was significantly correlated with negative impact to the patient and those around them across all SASNOS domains (rs range 0.42 - 0.45, all p ≤ 0.01). Conclusions: NBD is common within a subacute stroke inpatient population, particularly interpersonal and cognitive difficulties and preliminary analyses indicate associations with reduced functional ability, cognition and mood. There is a need to provide education and support to clinicians to facilitate routine assessment and management of NBD following stroke. [ABSTRACT FROM AUTHOR]

The relative safety of antidepressants during pregnancy has received substantial attention, but most syntheses fail to account for mental illness effects. We aimed to evaluate the literature comparing low birth weight (LBW) and neurodevelopmental and neurobehavioural outcomes for children whose mothers took antidepressants in pregnancy compared to those whose mothers had common mental disorders, or symptoms, but who did not take antidepressants during pregnancy. A systematic review was conducted searching PubMed, MEDLINE, PsycINFO and Embase in January 2015. A modified version of the Newcastle Ottawa Scale was used to assess study quality. Eleven cohort studies were included: four reporting a LBW outcome (all with higher risk of bias) and seven reporting a neurodevelopmental outcome (five with higher risk of bias). We found only limited evidence of gestational age-adjusted LBW in exposed children in two studies which had a higher risk of bias and did not control for depressive symptom severity. Only five (7.5%) neurodevelopmental outcomes and one (12.5%) neurobehavioural outcome showed evidence of a statistically significant effect, three out of four were from studies with a higher risk of bias. There is little robust evidence indicating a detrimental effect of antidepressant use during pregnancy on LBW and neurodevelopmental and neurobehavioural outcomes. More rigorous study designs are needed. [ABSTRACT FROM AUTHOR]

Cerebellar haemorrhage accounts for 5–10% of all intracerebral haemorrhages and leads to severe, long-lasting functional deficits. Currently, there is limited research on this stroke subtype, which may be due to the lack of a suitable composite neuroscoring system specific for cerebellar injury in rodents. The purpose of this study is to develop a comprehensive composite neuroscore test for cerebellar injury using a rat model of cerebellar haemorrhage. Sixty male Sprague-Dawley rats were subjected to either sham surgery or cerebellar haemorrhage. Twenty-four hours post-injury, neurological behaviour was evaluated using 17 cost-effective and easy-to-perform tests, and a composite neuroscore was developed. The composite neuroscore was then used to assess functional recovery over seven days after cerebellar haemorrhage. Differences in the composite neuroscore deficits for the mild and moderate cerebellar haemorrhage models were observed for up to five days post-ictus. Until now, a composite neuroscore for cerebellar injury was not available for rodent studies. Herein, using mild and moderate cerebellar haemorrhage rat models a composite neuroscore for cerebellar injury was developed and used to assess functional deficits after cerebellar haemorrhage. This composite neuroscore may also be useful for other cerebellar injury models. [ABSTRACT FROM AUTHOR]

Nicotine is a neuro-stimulant that has been implicated in the pathophysiology of many brain diseases. The need to prevent or alleviate the resulting dysfunction is therefore paramount, which has also given way to the use of medicinal plants in the management of brain conditions. This study was designed to determine the histomorphological and neurobehavioural changes in the cerebellum of Wistar rats following nicotine insult and how such injuries respond to Moringa intervention. Twenty-four adult male Wistar rats were divided into 4 groups. Group A and B were orally treated with normal saline and Moringa oleifera respectively for twenty-eight days; Group C was treated with nicotine while group D was treated orally with Moringa oleifera and intraperitoneally with nicotine for twenty-eight days. Animals were subjected to the open field test on the last day of treatment. 24 h after last day treatment, the animals were anesthetized and perfusion fixation was carried out. The cerebellum was excised and post-fixed in 4% paraformaldehyde and thereafter put through routine histological procedures. Results revealed cytoarchitectural distortion and extreme chromatolysis in neuronal cells of the cerebellar cortical layers in the nicotine-treated group. The Purkinje cells of the cerebellum of animals in this group were degenerated. There were also reduced locomotor activities in the group. Moringa was able to prevent the chromatolysis, distortion of the cerebellar cortical cells and neurobehavioural deficit. Our result suggests that Moringa oleifera could prevent nicotine-induced cerebellar injury in Wistar rats, with the possibility of ameliorating the clinical features presented in associated cerebellar pathology. [ABSTRACT FROM AUTHOR]

Aim: This study aimed to examine associations between structural MRI and concurrent motor, neurological and neurobehavioral measures at 30-32 weeks postmenstrual age (PMA; 'Early'), and at term equivalent age ('Term').Method: In this prospective cohort study, infants underwent Early MRI (n = 119; 73 male; median 32 weeks 1 day PMA) and Term MRI (n = 102; 61 male; median 40 weeks 4 days PMA) at 3 T. Structural images were scored generating white matter (WM), cortical gray matter, deep gray matter, cerebellar and global brain abnormality scores. Clinical measures were General Movements Assessment (GMs), Hammersmith Neonatal Neurological Examination (HNNE) and NICU Neonatal Neurobehavioral Scale (NNNS). The Premie-Neuro was administered Early and the Test of Infant Motor Performance (TIMP) and a visual assessment at Term.Results: Early MRI cerebellar scores were strongly associated with neurological components of HNNE (reflexes), NNNS (Hypertonicity), the Premie-Neuro neurological subscale (regression coefficient β = -0.06; 95% confidence interval CI = -0.09, -0.04; p < .001) and cramped-synchronized GMs (β = 1.10; 95%CI = 0.57, 1.63; p < .001). Term MRI WM and global scores were strongly associated with the TIMP (WM β = -1.02; 95%CI = -1.67, -0.36; p = .002; global β = -1.59; 95%CI = -2.62, -0.56; p = .001).Interpretation: Brain structure on Early and Term MRI was associated with concurrent motor, neurological and neurobehavioral function in very preterm infants. [ABSTRACT FROM AUTHOR]

Objectives: Mustard seeds, apart from being a culinary essential, have had medicinal applications dating back to the time of Hippocrates. It has in fact been once mentioned as the greatest herb ever. We explored the dose dependent effects of the crude aqueous extract of Brassica nigra (Black mustard seeds) on the prefrontal cortex of adult Wistar rats. Methods: 20 adult female rats weighing an average of 180±20 g were used. They were split into 4 groups (n=5); Group A (received extract at 200 mg/kg body weight), Group B (received extract at 100 mg/kg body weight), Group C (received extract at 50 mg/kg body weight), and Group D (received distilled water ad libitum). All of the animals were subjected to the Y-maze spontaneous alternation test for neurobehavioural analyses following 28-day administration of the extracts. Animals were sacrificed 24 hours after taking the last day of administration. Results: Our results showed that neurobehavioural analyses are significantly hampered in animals receiving 200 mg/kg extract in comparison to the control group. In treatment groups, increased dose of extract elevated the level of MDA, but reduced the level of SOD. LDH levels were also significantly increased in the 200 mg/kg treated group when comparing with the control. General microarchitecture in the prefrontal cortex of 200 mg/kg Brassica nigra treated group showed signs of karyolysis and pyknosis. Conclusion: Brassica nigra (black mustard) is not innocuous and therefore it should be consumed in moderation. [ABSTRACT FROM AUTHOR]

Psychiatric and cognitive impairment has been observed in premenopausal women with a hormonal disorder called polycystic ovary syndrome (PCOS). This study aimed to explore the possibility of combining pharmacological agents: Carvedilol and Clomiphene citrate, with antiestrogenic, antioxidant and anti-inflammatory properties in letrozole-induced PCOS rats. PCOS was induced in rats by the administration of letrozole (1 mg/kg) daily for 21 days. They were subsequently divided into four groups, each receiving either the vehicle or Clomiphene citrate (1 mg/kg) or Carvedilol or a combination of Clomiphene citrate and Carvedilol, respectively from days 22–36. Neurobehavioral studies were conducted on day 35 (Elevated plus maze and Y maze) and day 36 (Novel object recognition). The serum levels of the antioxidants Superoxide dismutase, Catalase, Interleukin 1B (IL-1B), and the gene expression of nuclear factor-erythroid factor 2-related factor 2 (Nrf2), Nuclear Factor k-Beta (NFKB), and acetylcholine esterase in the frontal brain homogenate was determined. Both Carvedilol and the combination therapy reversed the anxiety-like behavior, while Clomiphene citrate and the combination therapy ameliorated the spatial and non-spatial memory impairment observed in PCOS rats. Carvedilol, Clomiphene citrate, and the combination therapy increased the serum concentration of SOD and Catalase and decreased the serum concentration of IL-1B. The combination therapy up-regulated the NRF-2, NFKB, and acetylcholine esterase gene expression. Study showed that the combination of carvedilol and clomiphene citrate has anxiolytic potential and improved cognitive functions in PCOS rats. This might have been achieved by carvedilol and clomiphene citrate's ability to modulate the cholinergic system and the Nrf2 pathway while downregulating the NFκB signaling pathway. [ABSTRACT FROM AUTHOR]

Effects of sertraline, haloperidol or olanzapine administration on ketamine-induced behaviours in mice were examined. The aim was to ascertain the degree of reversal of such behaviours by sertraline, and compare its effectiveness to haloperidol and olanzapine. Ten-week old mice ( N = 120) were equally divided into main groups; 1 (open-field, radial-arm maze and elevated plus maze {EPM} tests), and 2 (social interaction test). Mice in each main group were assigned into six groups of ten ( n = 10) each. Group 1 received intraperitoneal (i.p) injection of vehicle, while groups 2-6 received i.p ketamine at 15 mg/kg daily for 10 days. From day 11 to 24, mice in group 1 (vehicle) were given distilled water (i.p at 2 ml/kg and oral at 10 ml/kg), group 2 (ketamine control) received daily i.p ketamine and oral distilled water; while animals in groups 3-6 received daily i.p. ketamine and oral haloperidol (4 mg/kg), olanzapine (2 mg/kg), or one of two doses of sertraline (SERT) (2.5 or 5 mg/kg), respectively. Treatments were administered daily, and behaviours assessed on days 11 and 24. Results showed that repeated ketamine administration caused hyperlocomotion, increased self-grooming, memory loss and social withdrawal. Administration of sertraline (both doses), haloperidol, and olanzapine reversed ketamine-induced behavioural changes. However, in the EPM, sertraline and olanzapine were anxiolytic, while haloperidol was anxiogenic. Sertraline's effect on behaviours tested was comparable to olanzapine and better than haloperidol. In conclusion, this study shows that sertraline's ability to counteract ketamine-induced behavioural changes in mice is comparable to known antipsychotics. [ABSTRACT FROM AUTHOR]

The present study aimed to elucidate the abnormalities in the development of rat brains, livers, kidney and behaviours after drinking desalinated seawater prenatally. Three types of drinking water were employed as an experimental probe (bottled water, filtered desalinated seawater and tap desalinated seawater) to investigate neurobehavioral and morphological changes in the development of pup rats. Female rats from each group were administered water from their birth until gestation and lactation. The 1st and 2nd generation pups were divided into three groups: Group C, mothers and pups administered with bottled drinking water (the control group); Group F, mothers and pups administered with filtered drinking water; Group T, mothers and pups administered with unfiltered desalinated seawater (tap water). Morphological changes (CNS aberration) and neurobehavioral changes were studied. The aberrations recorded in the tissues (brain, liver, kidney and spinal cord) of rats from groups T and F may be due to oxidative stress in these tissues such as reduced glutathione, lipid peroxidation, peroxidase and super oxide dismutase. In conclusion, drinking desalinated seawater for a long time may cause teratogenic effects in the development of New-born rats. [ABSTRACT FROM AUTHOR]

Objective We assessed the impacts of silymarin co-administration on aspartame-induced changes in novelty-induced behaviours, memory, anxiety-related behaviours, cerebral antioxidant status and histomorphology in mice. Method Six groups of mice were administered vehicle (distilled water), silymarin (25 mg/kg), aspartame (at 160 or 320 mg/kg), and silymarin (25 mg/kg) co-administered with aspartame at 160 or 320 mg/kg daily for 21 days, via an oral cannula. Behaviours were assessed after the first and last dose of treatment. Animals were sacrificed thereafter. Brain homogenates were used to assess antioxidant status; while sections of the cerebral cortex were processed for routine histology. Result Repeated co-administration of silymarin with aspartame resulted in significant suppression of horizontal locomotion and rearing, while grooming behaviour was enhanced; when compared to aspartame alone. Spatial working-memory showed significant improvement only after acute co-administration, while anxiety-related behaviours were reduced after repeated administration of both silymarin and aspartame. Cerebral cortical morphological integrity was better preserved, and astrocytic reactivity reduced with silymarin co-administration. Brain activity of superoxide dismutase and nitric oxide levels were decreased, while glutathione peroxidase activity was increased, when compared to levels seen with aspartame alone. Conclusion The study shows that co-administration of silymarin with aspartame was associated with significant attenuation of central effects, when compared to administration of aspartame alone. [ABSTRACT FROM AUTHOR]

Maternal weight before and during pregnancy is associated with offspring neurobehaviour in childhood. We investigated maternal weight prior to and during pregnancy in relation to neonatal neurobehaviour. We hypothesized that maternal obesity and excessive gestational weight gain would be associated with poor neonatal attention and affective functioning. Participants ( n = 261) were recruited, weighed and interviewed during their third trimester of pregnancy. Pre-pregnancy weight was self-reported and validated for 210 participants, with robust agreement with medical chart review ( r = 0.99). Neurobehaviour was measured with the NICU Network Neurobehavioural Scale (NNNS) administered on Days 2 and 32 postpartum. Maternal exclusion criteria included severe or persistent physical or mental health conditions (e.g. chronic disease or diagnoses of Bipolar Disorder or Psychotic Spectrum Disorders), excessive substance use, and social service/foster care involvement or difficulty understanding English. Infants were from singleton, full-term (37-42 weeks gestation) births with no major medical concerns. Outcome variables were summary scores on the NNNS ( n = 75-86). For women obese prior to pregnancy, those gaining in excess of Institute of Medicine guidelines had infants with poorer regulation, lower arousal and higher lethargy. There were no main effects of maternal pre-pregnancy body mass index on neurobehaviour. Women gaining above Institute of Medicine recommendations had neonates with better quality of movement. Additional studies to replicate and extend results past the neonatal period are needed. Results could support underlying mechanisms explaining associations between maternal perinatal weight and offspring outcomes. These mechanisms may inform future prevention/intervention strategies. © 2016 Blackwell Publishing Ltd [ABSTRACT FROM AUTHOR]

Changes, in behaviour, oxidative markers of stress and hippocampal morphology were evaluated following aspartame administration. Mice, (20–22 g each) were given vehicle (10 ml/kg) or aspartame (20, 40, 80 and 160 mg/kg) daily for 28 days. They were tested in the Y-maze, radial-arm maze and elevated plus-maze (EPM) after the first and last dose of vehicle or aspartame; and then sacrificed. Hippocampal slices were analysed for aspartic acid, nitric oxide (NO) and superoxide dismutase (SOD); and processed for general histology and neuritic plaques. Glial fibrillary-acid protein (GFAP) expression and neuron-specific enolase (NSE) activities were determined. Radial-arm maze scores increased significantly after acute administration at 80 and 160 mg/kg. Repeated administration at 20 and 40 mg/kg (Y-maze) and at 40 mg/kg (radial-arm maze) was also associated with increased scores, however, performance decreased at higher doses. EPM tests revealed anxiogenic responses following both acute and repeated administration. Significant increase in SOD and NO activities were observed at 40, 80 and 160 mg/kg. Neuron counts reduced at higher doses of aspartame. At 40, 80 and 160 mg/kg, fewer GFAP-reactive astrocytes were observed in the cornus ammonis, but increased GFAP-reactivity was observed in the dentate gyrus subgranular zone. NSE-positive neurons were readily identifiable within the dentate gyrus at the lower doses of aspartame; but at 160 mg/kg, there was marked neuron loss and reduction in NSE-positive neurons. Oral aspartame significantly altered behaviour, anti-oxidant status and morphology of the hippocampus in mice; also, it may probably trigger hippocampal adult neurogenesis. [ABSTRACT FROM AUTHOR]

Intake of herbs and some of their constituents is reported to reduce risks of some diseases, with Allium sativum being one of such. This study was conducted to investigate the effects of Allium sativum extract on the medial prefrontal cortex and neurobehaviour of adult Wistar rats. Twenty-four male Wistar rats were divided into 4 groups (n = 6). Group 1 was the control and received distilled water placebo orally, while groups 2-4 received oral doses of 78 mg/kg, 156 mg/kg and 312 mg/kg Allium sativum extract for 28 days. On day 29, spontaneous alternation behavioural test was carried out, and immediately the rats were anaesthetized (50 mg/kg ketamine hydrochloride IP.) and perfusion-fixed with 10% buffered formalin. The whole brains were removed and the medial prefrontal cortex excised and processed for histomorphologic studies by haematoxylin and eosin, and cresyl fast violet techniques. Neurobehavioural test revealed less spontaneous alternation in 156 mg/kg Allium sativum group, while the prefrontal cortices of the test groups showed hypertrophy, hyperplasia, pyknosis, karyorrhexis, chromatolysis, loss of brain cellular membranes and Nissl substance. The 156 mg/kg Allium sativum group showed altered spontaneous alternation, while cellular pathologic changes were observed in the medial prefrontal cortex of these test groups in a dose dependent sequence. [ABSTRACT FROM AUTHOR]

Mucopolysaccharidosis type IIIA (MPS IIIA) is an inherited metabolic disorder caused by a lysosomal enzyme deficiency resulting in heparan sulphate (HS) accumulation and manifests with a progressive neurodegenerative phenotype. A naturally occurring MPS IIIA mouse model is invaluable for preclinical evaluation of potential treatments but the ability to effectively assess neurological function has proved challenging. Here, the aim was to evaluate a set of behaviour tests for their reliability in assessing disease progression in the MPS IIIA mouse model. Compared to wild-type (WT) mice, MPS IIIA mice displayed memory and learning deficits in the water crossmaze from mid-stage disease and locomotor impairment in the hind-limb gait assessment at late-stage disease, supporting previous findings. Declined wellbeing was also observed in the MPS IIIA mice via burrowing and nest building evaluation at late-stage disease compared to WT mice, mirroring the progressive nature of neurological disease. Excessive HS accumulation observed in the MPS IIIA mouse brain from 1 month of age did not appear to manifest as abnormal behaviours until at least 6 months of age suggesting there may be a threshold of HS accumulation before measurable neurocognitive decline. Results obtained from the open field and three-chamber sociability test are inconsistent with previous studies and do not reflect MPS IIIA patient disease progression, suggesting these assessments are not reliable. In conclusion, water cross-maze, hind-limb gait, nest building and burrowing, are promising assessments in the MPS IIIA mouse model, which produce consistent results that mimic the human disease., Competing Interests: None., (© 2023 The Authors.)

Children who are born preterm are at risk of adverse long-term neurobehavioral outcomes, including cognitive, motor, and behavioral impairments. Early developmental interventions that commence within the first year after preterm birth have a preventative focus, with the aim to positively influence the developmental trajectory. While there is a great deal of heterogeneity in the research trials to date, there is evidence that early developmental interventions have a moderate effect on cognitive and behavioral outcomes up to preschool age, with some evidence for improved motor outcomes. This review discusses key components of early developmental interventions including commencing the intervention as early as possible, ideally in the neonatal intensive care unit, and promoting developmental skills overtime with an appropriate enriched environment. The importance of involving and supporting parents in early intervention is also highlighted, particularly given the influence of the parent–infant relationship on developmental outcomes and higher rates of mental health problems in parents after preterm birth. [ABSTRACT FROM AUTHOR]