Vanadium, a transition metal widely distributed in the environment, has been involved in neurotoxicity through oxidative stress and neuroinflammation. Chronic exposure may impair motor function, cognition, anxiety and depression-like behaviours, but the potential for recovery after withdrawal remains unclear especially in motor function, anxiety and depression-like behaviours. Male BALB/c mice were exposed to sodium metavanadate (3 mg/kg, intraperitoneal) for 3-, 9- or 15-months. Withdrawal groups received vanadium for 3-months followed by 6- or 12-months without exposure. Neurobehavioural assessments included motor coordination (inverted grid, beam walking), cognitive function (Y-maze), anxiety-like behaviour (open field) and depression-like behaviour (tail suspension test). Track and heat maps were used to visualize exploration and activity patterns. Chronic vanadium exposure induced progressive deficits in motor coordination, spatial memory, anxiety-like behaviour and depressive-like states. These impairments were most pronounced at 15-months of exposure. Withdrawal groups demonstrated partial recovery after 6-months and near-complete restoration after 12-months, with neurobehavioural performance approaching control levels across domains. Chronic vanadium exposure impairs motor, cognitive and affective functions in mice, but withdrawal promotes recovery, highlighting the reversibility of vanadium-induced neurotoxicity. These findings draw attention to the risks of chronic vanadium exposure while offering evidence that cessation can mitigate long-term neurobehavioural impairments.

This work was designed to investigate the morphometry and immunohistochemical features of pituitary glands in the African Giant Rats (AGR). Adult and juvenile AGR were sacrificed and their brains harvested, and the pituitary glands were carefully dissected. The weight, length and width of brains and pituitary glands were subsequently measured. Sections were prepared and stained using Haematoxylin and Eosin (H&E), Cresyl-violet and periodic-acid-Schiff (PAS) for histological analysis. Immunohistochemical analysis was carried out with Glial-Fibrillary-Acidic-Protein (GFAP) and Ionized-Calcium-Binding-Adapter-Molecule 1 (Iba1). Grossly, the AGR pituitary gland is a somehow laterally extended, saddle-shaped organ that is dorso-ventrally flattened. The gray-coloured adenohypophysis (anterior-pituitary lobe) was bigger in size than the whitish neurohypophysis (posterior-pituitary lobe) on physical examination. Histometrically, the adenohypophyseal length was noticeably greater than that of neurohypophysis in both juvenile and adult. Similarly, the adenohypophyseal and neurohypophyseal width in adult were found to be more than that of juvenile. Also, the histological staining of the neurohypophysis and adenohypophysis were distinct. In the neurohypophysis, fibrous and protoplasmic pituicytes were observed among fibres and Herring-bodies. Chromophils and chromophobes were identified in the adenohypophysis and melanotrophs in the intermediate lobe. Immunohistochemistry showed pituicytes in the neurohypophysis, which was positive with GFAP-antibody. With Iba1-antibody, the neurohypophysis expressed a stronger positive immunolabelling to microglia as compared to macrophages in the adenohypophysis. In conclusion, the gross and microscopic characteristics of pituitary glands of the AGR are found to be similar to other rodents and mammals. We recommend further study to compare morphometrical parameters between male and females of this model.

Traumatic Brain Injury (TBI) represents a major public health burden and a major contributor to disability and death, especially in the young population. It remains one of the most challenging human conditions to classify and the non-standardized classification is one of the numerous barriers in proper diagnosis and effective translation of experimental treatments in animal models. TBI is associated with numerous disorders, including amnesia, Parkinson's Disease, sleep disorders, Alzheimer's Disease, as well as disruption of physical, cognitive, and mental functioning. Several health care providers and the insurance industry see TBI as a singular 'event', meaning that the brain ''repairs'' over time, and does not require additional therapies. However, a single mild TBI can induce problems that self-propagate for months or years after the injury. There currently exist no diagnostic methods to quantify the extent of emotional and behavioral changes, cognitive impairment, fatigue, and sleep issues resulting from TBI in affected individual. The various animal and injury models available for TBI research are limited in clinical trials because a single TBI event is not fully understood. This review highlights the classifications of TBI, its heterogeneity, neuropathological lesions, long term sequelae, association with neurodegenerative disorders in human and animal studies, and attempts to modify the notion of TBI being viewed as a singular event.STATEMENT OF SIGNIFICANCE: The significance and strength of this review article lies in its comprehensive exploration of Traumatic Brain Injury (TBI) by addressing various factors that contribute to its complexity. We carried out a careful and detailed review of TBI classifications with an aim to provide a clearer and more detailed understanding of the heterogeneity inherent in these injuries. The examination of neuropathological lesions associated with TBI offers critical insights into the intricate nature of brain damage, fostering a deeper comprehension of the diverse outcomes resulting from TBI.Furthermore, this review critically evaluates the long-term sequelae of TBI, shedding light on the often-overlooked extended consequences that impact individuals well beyond the initial injury period. The findings from human and animal studies not only enriches our understanding of TBI but also highlights the translational implications for both clinical and preclinical research.A pivotal aspect of our review involves investigating the association between TBI and neurodegenerative disorders. By combining information from human studies and animal models, we aim to contribute to the growing body of knowledge that elucidates the intricate links between TBI and the development of neurodegenerative conditions.Most notably, this review challenges the conventional notion of TBI as a singular event by incorporating perspectives that emphasize its multifaceted nature. We critically assess attempts to modify this prevailing paradigm, encouraging a more nuanced understanding that considers the diverse manifestations and outcomes associated with TBI.In essence, this review endeavours to serve as a valuable resource for researchers, clinicians, and policymakers, fostering a comprehensive understanding of TBI that transcends traditional classifications and contributes to a more holistic approach in both research and clinical practice.

Environmental pollution due to heavy metal pollution is of growing concern, due to the increased industrial activities. The release of these substances into the atmosphere poses a great risk to humans, animals and the ecosystem at large. This study assesses the metal concentration levels of nine metals (lead, nickel, magnesium, cadmium, chromium, manganese, cobalt, copper and iron) in the sera and different brain regions (cerebellum, cerebrum and brainstem) of the hedgehog (Eulipotyphla), pigeon (Columbiformes), cattle egret (Pelecaniformes) and two species of the squirrel (sciuromorpha) using Atomic Absorption Spectrophotometry. Results obtained showed that of all the metals tested for, magnesium had the highest concentration across all samples and regions in all animals tested. Metal levels appeared to be higher than those reported in some previous studies from other climes, except for cobalt where there was no detectable level in all the tissues tested. Values obtained were highest in the serum, more than the brain. There was no particular pattern to the concentration of the metals in the brain regions. Data obtained from this study will serve as an indicator of the level of environmental pollution going on, and the long-term effect it can have on wildlife behavioural patterns and consequently the ecosystem.

Hydrocephalus, the aberrant enlargement of the brain's ventricles, is caused by a build-up of cerebrospinal fluid that stretches the periventricular white matter and may disrupt the connections between the pyramidal neurons in the cerebral cortex. Using an intra-cisternal kaolin injection hydrocephalic rat model, we aimed to determine if the effects of hydrocephalus on the white matter will subsequently impact the dendrites of cortical pyramidal neurons, which are the synaptic sites for the white matter fibres, particularly the afferent fibres. Three-week-old hydrocephalic rats were compared with controls after 1 week, 2 weeks and 4 weeks. Dendritic arborisations of the pyramidal neurons were evaluated using a modified Golgi stain. Haematoxylin and Eosin, and Cresyl violet stains were used to measure cortical thickness and pyramidal neuronal count. The hydrocephalic rats' cerebral cortex and corpus callosum were thinner (p<0.0001) than the controls. Rats with hydrocephalus had a similar pyramidal neuron count to the controls, with no significant decline. After two weeks of hydrocephalic induction, the pyramidal neurons' dendritic branching changed due to basal dendritic reduction and denudation. Reduced thickness in the corpus callosum and sensorimotor cortex was observed in the hydrocephalus animals. The pyramidal cell population remained unaffected, but the basal dendrites of the cells were substantially weakened. Ventricular enlargements during the juvenile developmental stage may harm dendritic arborization, which could obstruct neurological maturation.

Vanadium is a prevalent neurotoxic transition metal with therapeutic potentials in some neurological conditions. Hydrocephalus poses a major clinical burden in neurological practice in Africa. Its primary treatment (shunting) has complications, including infection and blockage; alternative drug-based therapies are therefore necessary. This study investigates the function and cytoarchitecture of motor and cerebellar cortices in juvenile hydrocephalic mice following treatment with varying doses of vanadium. Fifty juvenile mice were allocated into five groups (n = 10 each): controls, hydrocephalus-only, low- (0.15 mg/kg), moderate- (0.3 mg/kg), and high- (3.0 mg/kg) dose vanadium groups. Hydrocephalus was induced by the intracisternal injection of kaolin and sodium metavanadate administered by intraperitoneal injection 72hourly for 28 days. Neurobehavioral tests: open field, hanging wire, and pole tests, were carried out to assess locomotion, muscular strength, and motor coordination, respectively. The cerebral motor and the cerebellar cortices were processed for cresyl violet staining and immunohistochemistry for neurons (NeuN) and astrocytes (glial fibrillary acidic protein). Hydrocephalic mice exhibited body weight loss and behavioral deficits. Horizontal and vertical movements and latency to fall from hanging wire were significantly reduced, while latency to turn and descend the pole were prolonged in hydrocephalic mice, suggesting impaired motor ability; this was improved in vanadium-treated mice. Increased neuronal count, pyknotic cells, neurodegeneration and reactive astrogliosis were observed in the hydrocephalic mice. These were mostly mitigated in the vanadium-treated mice, except in the high-dose group where astrogliosis persisted. These results demonstrate a neuroprotective potential of vanadium administration in hydrocephalus. The molecular basis of these effects needs further exploration. The neuroprotective potentials of varying doses of vanadium were studied in an experimental model of hydrocephalus. All doses improved motor function, restored neuronal and glial count, and architecture; however, the high dose resulted in persistent astrocytic reactivity.image

Background:The hippocampal alterations resulting from hydrocephalus are associated with various cognitive dysfunctions. Reduced learning and memory are early functional deficits that recover with time in experimental hydrocephalus. This study investigated the recovery processes of learning and memory loss in relation to the morphology of hippocampal pyramidal neurons and the degree of expansion of the ventricles. Materials and Methods:Hydrocephalus was induced in adult mice by intracisternal injection of sterile kaolin while controls received sham operation. Neurobehavioral tests for memory and learning were conducted, after which the animals were sacrificed in batches: 7 (acute) and 28 (subacute) days postinduction. After sacrifice, mice were categorized into mild and moderate hydrocephalus, and their fixed brain samples were processed for hematoxylin, eosin, and Nissl stains. Results:In moderate acute hydrocephalus, the indices of learning and memory were reduced escape latency (67.20 ± 12.83 s), number of platform crossing (4.000 ± 1.658), duration in platform quadrant (4.000 ± 1.658), and percent of total investigation (44.857% ± 3.981%) but not in the subacute stage. Pyknotic indices (PI) were significantly higher in the cornu ammonis (CA)1 and 3 regions in all hydrocephalic groups than in controls. However, within groups, PI was significantly higher only in the CA1 of moderate acute (28.149% ± 1.875%) compared to moderate subacute hydrocephalic group (12.903% ± 3.23%). Conclusion:Hydrocephalus caused cellular injury to the hippocampus associated with spatial learning and memory deficits. However, these functional deficits were partially reversed in moderate subacute hydrocephalus despite the persistence of the structural alterations in the CA1 and CA3 subregions.

Vanadium is a widely used transition metal in industrial applications, but it also poses significant neurotoxic and environmental risks. Previous studies have shown that exposure to vanadium may lead to neurodegenerative diseases and neuropathic pain, raising concerns about its impact on human health and the ecosystem. To address vanadium neurotoxicity, through targeting NMDA glutamate and dopamine signaling, both involved in neurodegenerative disorders, shows promise. Using Caenorhabditis elegans as a model, we evaluated a novel compound with a mixed NMDA glutamate receptor-dopamine transporter pharmacology, ZA-II-05 and found it effectively ameliorated vanadium-induced neurotoxicity, suggesting a potential neuroprotective role. Synchronized young adult worms were assigned to four different experimental groups; Controls; 100 mM of Vanadium; Vanadium and 1 mg/ml ZA-II-05; and ZA-II-05 alone. These were examined with different markers, including DAPI, MitoTracker Green and MitoSox stains for assessment of nuclei and mitochondrial density and oxidative stress, respectively. Exposure to vanadium in C. elegans resulted in decreased nuclear presence and reduction in mitochondrial content were also analyzed based on fluorescence in the pharyngeal region, signifying an increase in the production of reactive oxygen species, while vanadium co-treatment with ZA-II-05 caused a significant increase in nuclear presence and mitochondrial content. Treatment with ZA-II-05 significantly preserved cellular integrity, exhibiting a reversal of the detrimental effects induced by vanadium by modulating and preserving the normal function of chemosensory neurons and downstream signaling pathways. This study provides valuable insights into the mechanisms of vanadium-induced neurotoxicity and offers perspectives for developing therapeutic interventions for neurodegenerative diseases related to environmental toxins.

Background: Hippocampus is a neural structure in the temporal lobe that plays a crucial role in learning and memory. Cognitive impairment with learning disabilities is a common feature in hydrocephalus and is more prominent in adult-onset hydrocephalus. The aim of this study is to describethe morphological alterations in the pyramidal cells of the hippocampus of adult hydrocephalic mice. Method: Hydrocephalus was induced in adult albino mice by intra-cisternal injection of kaolin suspension (250 mg/ml in sterile water). They were sacrificed 7, 14 and 21 days post-induction. Morphological analysis was carried out on hematoxylin and eosinstained coronal sections of the hippocampus: the pyramidal neurons (normal and pyknotic) in the CA1 and CA3 subregions were counted and the pyknotic index (PI) was calculated. The somatic and dendritic features of Golgistained pyramidal neurons were examined by light microscopy in both hydrocephalic and control mice. Result: The PI was significantly greater in the CA1 region of the hippocampus in the hydrocephalic groups compared to the agematched controls. The dendritic processes of pyramidal neurons in the CA1 region were fewer with shorter terminal branches in the hydrocephalic mice than in controls; this was pronounced at 7 days post-induction. In the CA3 region, there was no difference in dendritic arborization between hydrocephalic and control mice. Conclusion: Acute adult-onset hydrocephalus was associated with increased pyknosis and reduced dendritic arborization in hippocampal pyramidal cells in the CA1 but not CA3 region. Keywords: Hippocampal pyramidal cell, Hydrocephalus, Pyknotic index, Golgi stain

The subcommissural organ (SCO) is a well-developed gland present in the brain of vertebrates. The SCO secretes glycoproteins into the circulating cerebrospinal fluid and these assemble to form Reissner's fibre. It also plays an important function in neurogenesis and axonal guidance during embryogenesis. This study delves into the microscopic anatomy of the SCO in the adult greater cane rat (GCR), shedding light on its histoarchitectural characteristics. By utilizing histological techniques and microscopic analysis, we investigated the SCO's location and cellular composition within the brain of adult GCR. Our findings showed that the SCO in this species is located ventrally to the posterior commissure (PC) and dorsally to the third ventricle. The SCO consists of specialized ependymal or nuclear cell layer and apical processes lining the third ventricle. Moreover, the SCO's proximity to the PC and the third ventricle highlights its strategic position within the brain's ventricular system. With immunohistochemical analyses, the SCO cells expressed glial fibrillary protein when immunolabelled with Glial fibrillary acid protein (GFAP) antibody, a marker for astrocytes/astrocytic-like cells. Few microglia-like cells were immuno-positive for Ionized calcium-binding adapter molecule 1 (Iba1) antibody, that are existing within the SCO. However, the SCO in the GCR showed a negative immunostaining to NeuN antibody. This study contributes to our understanding of the microscopic anatomy of the SCO in a lesser-studied mammalian species. Further research into the SCO's functional significance especially during development in the GCR, may hold promise for more insights into neurological health and pathology.

Pollution by heavy metals is a threat to public health because of the adverse effects on multiple organ systems including the brain. Here, we used the African giant rat (AGR) as a novel sentinel host to assess the effect of heavy metal accumulation and consequential neuropathology upon the brain. For this study, AGR were collected from distinct geographical regions of Nigeria: the rain forest region of south-west Nigeria (Ibadan), the central north of Nigeria (Abuja), and in oil-polluted areas of south Nigeria (Port-Harcourt). We found that zinc, copper, and iron were the major heavy metals that accumulated in the brain and serum of sentinel AGR, with the level of iron highest in animals from Port-Harcourt and least in animals from Abuja. Brain pathology, determined by immunohistochemistry markers of inflammation and oxidative stress, was most severe in animals from Port Harcourt followed by those from Abuja and those from Ibadan were the least affected. The brain pathologies were characterized by elevated brain advanced oxidation protein product (AOPP) levels, neuronal depletion in the prefrontal cortex, severe reactive astrogliosis in the hippocampus and cerebellar white matter, demyelination in the subcortical white matter and cerebellar white matter, and tauopathies. Selective vulnerabilities of different brain regions to heavy metal pollution in the AGR collected from the different regions of the country were evident. In conclusion, we propose that neuropathologies associated with redox dyshomeostasis because of environmental pollution may be localized and contextual, even in a heavily polluted environment. This novel study also highlights African giant rats as suitable epidemiological sentinels for use in ecotoxicological studies.

N-methyl-D-aspartate receptors (NMDARs) are ion channels that respond to the neurotransmitter glutamate, playing a crucial role in the permeability of calcium ions and excitatory neurotransmission in the central nervous system (CNS). Composed of various subunits, NMDARs are predominantly formed by two obligatory GluN1 subunits (with eight splice variants) along with regulatory subunits GluN2 (GluN2A-2D) and GluN3 (GluN3A-B). They are widely distributed throughout the CNS and are involved in essential functions such as synaptic transmission, learning, memory, plasticity, and excitotoxicity. The presence of GluN2A and GluN2B subunits is particularly important for cognitive processes and has been strongly implicated in neurodegenerative diseases like Parkinson's disease and Alzheimer's disease. Understanding the roles of GluN2A and GluN2B NMDARs in neuropathologies provides valuable insights into the underlying causes and complexities of major nervous system disorders. This knowledge is vital for the development of selective antagonists targeting GluN2A and GluN2B subunits using pharmacological and molecular methods. Such antagonists represent a promising class of NMDA receptor inhibitors that have the potential to be developed into neuroprotective drugs with optimal therapeutic profiles.

Vanadium is a ubiquitous transition metal that has been generating contrasting research interest. Therapeutically, vanadium possess antidiabetic, antitumor, antiparasitic and even neuroprotective activities. On the flip side, vanadium has been reported to cause multisystemic toxicities with a strong predilection for the nervous system. Despite several reports on potential benefits of low-dose vanadium (LDV) and toxic effects of high-dose vanadium (HDV), there are no comparative studies done thus far. This study therefore explored the comparative effects of LDV and HDV exposure in mice during postnatal development. A total of nine (9) nursing mice were used in this study; with three nursing mice and their pups (n = 12 pups per group) randomly assigned to each of the three test groups. The nursing dam were given intraperitoneal (i.p) injection of vanadium at 0.15mg/kg and 3mg/kg for LDV and HDV respectively, and subseqently to the pups from postnatal day (PND) 15 till sacrifice on PND 90. We discovered that neurodevelopmental motor function test of mice-pups exposed to LDV here showed improved motor development, muscular strength and memory capacities whereas HDV led to motor function impairment, reduced muscular strength and memory capacities.  LDV-exposed mice showed mild histological lesions in cerebral cortex whereas high-dose showed distinct histological lesions in different parts of the brain ranging from cerebellar Purkinje neuronal pathology (central chromatolysis), pyramidal neuronal loss in CA1 region, architectural distortion as well as fewer neurons in olfactory bulb. We saw mild lesions with LDV in both liver and kidney, however, with HDV exposure, there was diffuse hepatocellular vacuolar degeneration and congestion of blood vessels in liver, shrinkage of renal glomerulus and degenerated epithelial cells of kidney. Conclusively, beneficial effect of vanadium is proven as it facilitated body weight gain which translate in organ weight at low-dose, while high-dose caused decreased neurobehaviour and histological lesions.

Background:Hydrocephalus is a neurological condition known to cause learning and memory disabilities due to its damaging effect on the hippocampal neurons, especially pyramidal neurons. Vanadium at low doses has been observed to improve learning and memory abilities in neurological disorders but it is uncertain whether such protection will be provided in hydrocephalus. We investigated the morphology of hippocampal pyramidal neurons and neurobehavior in vanadium-treated and control juvenile hydrocephalic mice.Methods:Hydrocephalus was induced by intra-cisternal injection of sterile-kaolin into juvenile mice which were then allocated into 4 groups of 10 pups each, with one group serving as an untreated hydrocephalic control while others were treated with 0.15, 0.3 and 3 mg/kg i.p of vanadium compound respectively, starting 7 days post-induction for 28 days. Non-hydrocephalic sham controls (n = 10) were sham operated without any treatment. Mice were weighed before dosing and sacrifice. Y-maze, Morris Water Maze and Novel Object Recognition tests were carried out before the sacrifice, the brains harvested, and processed for Cresyl Violet and immunohistochemistry for neurons (NeuN) and astrocytes (GFAP). The pyramidal neurons of the CA1 and CA3 regions of the hippocampus were assessed qualitatively and quantitatively. Data were analyzed using GraphPad prism 8.Results:Escape latencies of vanadium-treated groups were significantly shorter (45.30 ± 26.30 s, 46.50 ± 26.35 s, 42.99 ± 18.44 s) than untreated group (62.06 ± 24.02 s) suggesting improvements in learning abilities. Time spent in the correct quadrant was significantly shorter in the untreated group (21.19 ± 4.15 s) compared to control (34.15 ± 9.44 s) and 3 mg/kg vanadium-treated group (34.35 ± 9.74 s). Recognition index and mean % alternation were lowest in untreated group (p = 0.0431, p=0.0158) suggesting memory impairments, with insignificant improvements in vanadium-treated groups. NeuN immuno-stained CA1 revealed loss of apical dendrites of the pyramidal cells in untreated hydrocephalus group relative to control and a gradual reversal attempt in the vanadium-treated groups. Astrocytic activation (GFAP stain) in the untreated hydrocephalus group were attenuated in the vanadium-treated groups under the GFAP stain. Pyknotic index in CA1 pyramidal layer of untreated (18.82 ± 2.59) and 0.15mg/kg vanadium-treated groups (18.14 ± 5.92) were significantly higher than control (11.11 ± 0.93; p = 0.0205, p = 0.0373) while there was no significant difference in CA3 pyknotic index across all groups.Conclusion:Our results suggest that vanadium has a dose-dependent protective effect on the pyramidal cells of the hippocampus and on memory and spatial learning functions in juvenile hydrocephalic mice.

Exposure to heavy metals, such as vanadium, poses an ongoing environmental and health threat, heightening the risk of neurodegenerative disorders. While several compounds have shown promise in mitigating vanadium toxicity, their efficacy is limited. Effective strategies involve targeting specific subunits of the NMDA receptor, a glutamate receptor linked to neurodegenerative conditions. The potential neuroprotective effects of ZA-II-05, an NMDA receptor antagonist, against vanadium-induced neurotoxicity were explored in this study. Organotypic rat hippocampal slices, and live mice, were used as models to comprehensively evaluate the compound’s impact. Targeted in vivo fluorescence analyses of the hippocampal slices using propidium iodide as a marker for cell death was utilized. The in vivo study involved five dams, each with eight pups, which were randomly assigned to five experimental groups (n = 8 pups). After administering treatments intraperitoneally over six months, various brain regions were assessed for neuropathologies using different immunohistochemical markers. High fluorescence intensity was observed in the hippocampal slices treated with vanadium, signifying cell death. Vanadium-exposed mice exhibited demyelination, microgliosis, and neuronal cell loss. Significantly, treatment with ZA-II-05 resulted in reduced cellular death in the rat hippocampal slices and preserved cellular integrity and morphological architecture in different anatomical regions, suggesting its potential in countering vanadium-induced neurotoxicity.

We studied the pyramidal neurons of the hippocampus in neonatal, juvenile and adult rats with hydrocephalus of varying durations and related these changes to their learning and memory. Hydrocephalus was induced in 7-day-old neonates, 4-week-old juvenile and 16-week-old adult Albino rats by intra-cisternal injection 0.02-0.04 ml of 150mg/ml of kaolin in sterile water (150 mg/ml). We studied escape latency and platform crossings with the Morris water maze prior to animal sacrifice at 2 and 4 weeks post induction in neonates and at 4 and 8 weeks post induction in juveniles and adults. We examined pyramidal neurons with cresyl violet and modified Golgi stain and analyzed behavioural scores and pyknotic indices. Statistical significance was determined at p<0.05. The basal dendrites of the pyramidal neurons were reduced in the hydrocephalic groups. In the CA1, the pyknotic index was significantly increased in both groups of hydrocephalic neonates but only in hydrocephalic juveniles and adults sacrificed at 4 weeks. In the CA3 it was increased in hydrocephalic neonates sacrificed at 2 weeks and hydrocephalic juveniles sacrificed at 4 weeks. The escape latency was greater and the number of platform crossing was lower in the hydrocephalic rats than in their age matched controls. Pyramidal neurons were morphologically altered in hydrocephalus, in association with changes in spatial learning and memory. The CA1 region in young animals was particularly vulnerable. Functional recovery occurs with time and to a greater extent in older animals.

Background: Hydrocephalus is currently managed by cerebrospinal fluid diversion from the cerebral ventricles to other body sites, but this is complicated by obstruction and infection in young infants, thus adding to morbidity and mortality. Studies have reported caffeine to be a pleiotropic neuroprotective drug in the developing brain due to its antioxidant, anti-inflammatory, and antiapoptotic properties, with improved white matter microstructural development. In this study, we investigate the use of caffeine administration as a possible means of pharmacological management for hydrocephalus.Methods: A total of 76 three-day-old mice pups from 10 dams were divided into four groups: hydro-cephalus was induced in the pups in two groups by intracisternal injection of kaolin suspension, and their dams were given either caffeine (50 mg/kg by gavage) or water daily for 21 days; the dams in the other 2 (non-hydrocephalic) groups similarly had either caffeine or water; the pups received caffeine administered via lactation. Developmental neurobehavioral tests were performed until day 21, when the pups were sacrificed. Their brains were removed and processed for Cresyl and Golgi staining; both quantitative and qualitative analyses were then carried out. Results: Improved developmental motor activities and reflexes were observed in the hydrocephalus thorn caffeine-treated pups. Caffeine administration was associated with reduced cell death and increased dendritic arborization of the neurons in the sensorimotor cortex and striatum of hydrocephalic mice pups.Conclusion: Caffeine administration appears to have promise as an adjunct in hydrocephalus management, and its use needs to be further explored. (c) 2022 Elsevier Inc. All rights reserved.

The incidence of spinal cord (SC) injury in developed and undeveloped countries is alarming. The pig (Sus scrofa) has been recommended as a suitable research model for translational studies because of its morphophysiological similarities of organ systems with humans. There is a dearth of information on the SC anatomy of the large white and landrace crossbreed (LW-LC) pigs. We therefore aim to describe the gross morphology and morphometry of its SC. Twelve juvenile LW-LC pigs (six males and six females) were used. The skin and epaxial muscles were dissected to expose the vertebral column. The SC was carefully harvested by laminectomy, and 13 gross SC morphometric parameters were evaluated. Thirty-three spinal nerves were seen emanating from either side of the SC by means of dorsal and ventral spinal roots. The overall average of SC length and weight was 36.23 ± 1.01 cm and 16.60 ± 0.58 g, respectively. However, the mean SC length and weight were higher in females compared with males, with SC weight being statistically significant. A positive relationship between SC length and weight was significant for males (p = 0.0435) but not for females (p = 0.42). Likewise, the strength of the relationship between SC length and weight was significant in males (r = 0.82) but not significant in females (r = 0.41). Baseline data for the morphometric features of the spinal cord in the LW-LC pigs were generated, which will contribute to the knowledge of this species anatomy and useful information on regional anaesthesia that should further strengthen the drive in adopting the pig as a suitable research model for biomedical research.