Department of Anatomy

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Ascorbic Acid Ameliorates Behavioural Deficits and Neuropathological Alterations in Rat Model of Alzheimer’s Disease
(Elsevier Ltd, 2017-02) Yawson, Emmanuel
Exploring the links between neural pathobiology and behavioural deficits in Alzheimer's disease (AD), and investigating substances with known therapeutic advantages over subcellular mechanisms underlying these dysfunctions could advance the development of potent therapeutic molecules for AD treatment. Here we investigated the efficacy of ascorbic acid (AA) in reversing aluminium chloride (AlCl3)-induced behavioural deficits and neurotoxic cascades within prefrontal cortex (PFC) and hippocampus of rats. A group of rats administered oral AlCl3 (100mg/kg) daily for 15days showed degenerative changes characterised by significant weight loss, reduced exploratory/working memory, frontal-dependent motor deficits, cognitive decline, memory dysfunction and anxiety during behavioural assessments compared to control. Subsequent analysis showed that oxidative impairment-indicated by depleted superoxide dismutase and lipid peroxidation (related to glutathione-S-transferase activity), cholinergic deficits seen by increased neural acetylcholinesterase (AChE) expression and elevated lactate dehydrogenase underlie behavioural alterations. Furthermore, evidences of proteolysis were seen by reduced Nissl profiles in neuronal axons and dendrites which correspond to apoptotic changes observed in H&E staining of PFC and hippocampal sections. Interestingly, AA (100mg/kg daily for 15days) significantly attenuated behavioural deficits in rats through inhibition of molecular and cellular stressor proteins activated by AlCl3. Our results showed that the primary mechanisms underlying AA therapeutic advantages relates closely with its abilities to scavenge free radicals, prevent membrane lipid peroxidation, modulate neuronal bioenergetics, act as AChE inhibitor and through its anti-proteolytic properties. These findings suggest that supplementing endogenous AA capacity through its pharmacological intake may inhibit progression of AD-related neurodegenerative processes and behavioural alterations.
Behavioural Cellular and Neurochemical Alterations in Rat Prefrontal cortex and Hippocampus Exposed to Tigernut (Cyperus esculentus) Treatment
(2018-12) Yawson, Emmanuel
Investigating substances of plant origin for therapeutic advantages over subcellular mechanisms underlying a number of physiological dysfunctions could foster the development of potent therapeutic strategies for the treatment of these dysfunctions. We explored the effects of Tigernut (Cyperus esculentus) consumption on neurochemical, behavioural and cellular parameters in prefrontal and hippocampal regions of rat brain. Twenty-four (24) adult male Wistar rats with an average weight of 180g±10g were randomly split into 4 (A-D) groups (n=6); Groups A – C received 10mg/kg, 20mg/kg, and 30mg/kg bodyweight of Tigernut extract respectively for 14days, while Group D served as the control receiving distilled water. Animals were sacrificed 24hours after the last day of administration. Behavioural assessment of the cortico-hippocampal neural circuitry in Tigernut–treated rats showed increased memory function compared to control, evidenced by an increase in correct spontaneous alternation in the Tigernut-treated groups. Neural malondialdehyde (MDA) levels was significantly reduced in treated rats in order of increasing dose, while the concentrations of catalase (CAT) and superoxide dismutase (SOD) were significantly increased. These observations hinted at the antioxidant properties of Tigernut. Subsequent analysis of the total antioxidant capacity in animals revealed elevated antioxidant levels significantly in the 10mg/kg and 20mg/kg groups. Furthermore, the microarchitecture of the prefrontal cortex and hippocampus appeared normal and well-structured. Our results show that Tigernut has neurotherapeutic and antioxidant properties at moderate doses and can therefore, be used to augment the endogenous production of antioxidants in the different brain regions
The Cerebellum under Stress: Dietary African Walnut (Tetracarpidium conophorum) Abrogates Oxidative Stress-driven Neuropathology Induced by Chronic Unpredictable Stress
(2021-03) Yawson, Emmanuel
Background: Consumption of a healthy diet abundant in antioxidant and anti-inflammatory phytochemicals, offers an effective and least expensive way to prevent neurodegeneration. Herein, the role of Tetracarpidium conophorum (African walnut) enriched diet in chronic stress-induced cerebellar neuropathology was investigated Methodology: Twenty-one male Wistar rats were used for this investigation. Rats were randomly assigned into three groups (A, B, and C), each consisting of 7 rats (n = 7). Group A (Control group) were fed control diet; group B rats were subjected to different chronic unpredictable stressors (CUS) + control diet for 21 days, while group C rats were subjected to CUS + Walnut-enriched diet for 21 days. Serum corticosterone levels, the expression level of antioxidant and inflammatory markers, and cytoarchitectural changes in cerebellum were assessed by enzyme-linked immunosorbent assay (ELISA) immunohistochemistry methods. Results: The walnut-enriched diet prevented astrogliosis, modulated serum corticosterone expression, and tumor necrotic factor-α in the cerebellum. The walnut-enriched diet also caused an improvement in the antioxidant profile, indicating that it suppressed chronic unpredictable stress-induced perturbations. Conclusion: Our results suggest that African walnut exerts protective effects against oxidative stress-driven dysfunction by reducing serum corticosterone levels, modulating oxidative stress pathways, and preventing neuronal morphological damage in the cerebellum.
Comparison of Indices of Insulin Resistance and Islet Beta-Cell Dysfunction across Rat Models of Diabetes Mellitus Induced by Modified Diets or Streptozotocin
(2018-04) Yawson, Emmanuel
Background: Induction of insulin resistance in rodents involves the use of Streptozotocin (STZ) or diets high in sucrose, fat or fructose; but the relative degrees of insulin resistance induced by each of these approaches are unclear. Aim and Objectives: We therefore compared the degree to which intraperitoneal STZ with or without high-fat or high-fructose diet would induce insulin resistance, glucose intolerance and islet β-cell dysfunction in Wistar rats. Materials and Methods: Subsets of STZ-injected rats administered streptozotocin at 30 mg/kg body weight for five successive days were fed normal diet (STZ), or diets high in fat or fructose for 30 or 60 days. Normoglycaemic rats on normal rodent chow, High Fat Diet (HFD) or High Fructose Drink (HFrD) constituted the control (CTR), HFD or HFrD groups, respectively. Rats were anaesthetized and sacrificed at 30 or 60 days of high fat or fructose feeding followed by measurement of fasting plasma glucose and insulin; and calculation of the HOMA-IR and HOMA-%β. Oral Glucose Tolerance Test (OGTT) was done 48 hours prior to killing the animals. Results: Glucose tolerance and islet β-cell function were most severely perturbed in the STZ-injected hyperglycaemic rats fed diets high in fructose or fat, as indicated by the significantly increased (p<0.05) HOMA-IR or decreased HOMA%β (p<0.05) at 30 or 60 days compared with the CTR, STZ or diet-only groups. Weekly blood glucose was most markedly and significantly (p<0.05) elevated in these same (STZ+diet) groups, with impaired OGTT. Conclusion: The profound impairment of glucose tolerance and β-cell function in the STZ-induced hyperglycemic rats fed high-fat or high-fructose diet support the continued use of such models in the characterization of the molecular events associated with insulin resistance, and the testing of novel therapeutic interventions.
Depression in Sub-Saharan Africa
(Elsevier Ltd, 2022-06) Yawson, Emmanuel
Mood disorders can be considered among the most common and debilitating mental disorders. Major depression, as an example of mood disorders, is known to severely reduce the quality of life as well as psychosocial functioning of those affected. Its impact on the burden of disease worldwide has been enormous, with the World Health Organization projecting depression to be the leading cause of mental illness by 2030. Despite several studies on the subject, little has been done to contextualize the condition in Africa, coupled with the fact that there is still much to be understood on the subject. This review attempts to she d more light on the prevalence of depression in Sub-Saharan Africa (SSA), its pathophysiology, risk factors, diagnosis and the experimental models available to study depression within the sub-region. It also evaluates the contribution of the sub-region to the global research output of depression as well as bottlenecks associated with full exploitation of the sub region’s resources to manage the disorder.
Hippocampal Cellular Changes in Androgen Deprived Insulin Resistant Rats
(Springer Nature Switzerland AG, 2021-06) Yawson, Emmanuel
Androgen deprivation can be achieved through testosterone antagonists (chemical castration) with or without orchidectomy. We use a rat model to characterize hippocampal structural and functional changes that might be associated with a subset population of androgen deprived insulin-resistant patients. Adult male Wistar rats assigned into six (6) groups: control group (distilled water/sham), orchiectomy group (bilateral orchiectomy), flutamide group (oral flutamide; 11 mg/kg body weight), diabetes group (multiple low-dose of streptozotocin (STZ; 30 mg/kg body weight intraperitoneally), orchiectomy and diabetic group (bilateral orchiectomy with 30 mg/kg body weight of STZ), and orchiectomy/diabetic/flutamide group (bilateral orchiectomy with 30 mg/kg body weight of STZ with 11 mg/kg body weight of flutamide). Animals were sacrificed at 30 and 60 days respectively. Spatial learning and working memory behavior were assessed; while total plasma; testosterone, insulin levels, and fasting blood glucose were assayed; the Homeostasis model for insulin resistance was also calculated. Histological examinations by H&E and CFV, while immunohistochemical analysis of astrocytes, P53 protein, and NSE were performed. Androgen deprived insulin-resistant state caused altered learning and cognitive behavior through decreased percentage correct alternation to an increased escape latency period. Significant bidirectional correlates exist between the hormonal profiles relative to the control group (p < 0.05), especially in the 60 days post-orchiectomy. While histological and immunohistochemical data indicate microcellular derangement. That the summate effects of androgen deprivation and impaired insulin signaling exacerbate hippocampal neurodegenerative changes that merit further studies.
Hippocampal Degeneration and Behavioral Impairment During Alzheimer-Like Pathogenesis Involves Glutamate Excitotoxicity
(Springer, 2021-01-08) Yawson, Emmanuel
The hallmarks of Alzheimer’s disease (AD) pathology include senile plaques accumulation and neurofibrillary tangles, which is thought to underlie synaptic failure. Recent evidence however supports that synaptic failure in AD may instead be instigated by enhanced N-methyl-D-aspartate (NMDA) activity, via a reciprocal relationship between soluble amyloid-β (Aβ) accumulation and increased glutamate agonist. While previous studies have shown Aβ-mediated alterations to the glutamatergic system during AD, the underlying etiology of excitotoxic glutamate-induced changes has not been explored. Here, we investigated the acute effects of stereotaxic dentate gyrus (DG) glutamate injection on behavior and molecular expression of specific proteins and neurochemicals modulating hippocampal functions. Dependence of glutamate-mediated effects on NMDA receptor (NMDAR) hyperactivation was tested using NMDARs antagonist memantine. DG of Wistar rats (12-weeks-old) were bilaterally microinjected with glutamate (500 mM) with or without daily intraperitoneal (i.p.) memantine injection (20 mg/kg) for 14 days, while controls received either intrahippocampal/i.p. PBS or i.p. memantine. Behavioral characterization in open field and Y-maze revealed that glutamate evoked anxiogenic responses and perturbed spatial memory were inhibited by memantine. In glutamate-treated rats, increased NO expression was accompanied by marked reduction in profiles of glutathione-s-transferase and glutathione peroxidase. Similarly, glutamatemediated increase in acetylcholinesterase expression corroborated downregulation of synaptophysin and PSD-95, coupled with initiation of reactive astrogliosis (GFAP). While neurofilament immunolocalization/immunoexpression was unperturbed, we found glutamate-mediated reduction in neurogenic markers Ki67 and PCNA immunoexpression, with a decrease in NR2B protein expression, whereas mGluR1 remains unchanged. In addition, increased expression of apoptotic regulatory proteins p53 and Bax was seen in glutamate infused rats, corroborating chromatolytic degeneration of granule neurons in the DG. Interestingly, memantine abrogated most of the degenerative changes associated with glutamate excitotoxicity in this study. Taken together, our findings causally link acute glutamate dyshomeostasis in the DG with development of AD-related behavioral impairment and molecular neurodegeneration.
Inhibitory Potentials of Cymbopogon citratus Oil against Aluminium-induced Behavioral Deficits and Neuropathology in Rats
(Anatomy and cell biology, 2020-09) Yawson, Emmanuel
Cymbopogon citratus is a tropical phytomedicinal plant that is widely known for its hypoglycemic, hypolipidemic, anxiolytic, sedative, antioxidative and anti-inflammatory properties. In this study, we have examined the neuroprotective effects of the essential oil (ESO) of Cymbopogon citratus, following aluminum chloride (AlCl3)-induced neurotoxicity within the cerebellum of Wistar rats. A total of 40 adult male Wistar rats were assigned into five groups and treated orally as follows: A–phosphate-buffered saline (1 ml daily for 15 days); B–ESO (50 mg/kg daily for 15 days); C–AlCl3 (100 mg/kg daily for 15 days); D–AlCl3 then ESO (100 mg/kg AlCl3 daily for 15 days followed by 50 mg/kg ESO daily for subsequent 15 days); E–ESO then AlCl3 (50 mg/kg ESO daily for 15 days followed by 100 mg/kg AlCl3 daily for following 15 days). To address our questions, we observed the locomotion and exploratory behavior of the rats in the open field apparatus and subsequently evaluated cerebellar oxidative redox parameters, neural bioenergetics, acetylcholinesterase levels, transferrin receptor protein, and total protein profiles by biochemical assays. Furthermore, we investigated cerebellar histomorphology and Nissl profile by H&E and Cresyl violet Nissl staining procedures. ESO treatment markedly attenuated deficits in exploratory activities and rearing behavior following AlCl3 toxicity, indicating its anxiolytic potentials. Additionally, AlCl3 evoked increase in malondialdehyde and nitric oxide levels, as well as repressed cerebellar catalase, glutathione peroxidase, and superoxide dismutase profiles were normalized to baseline levels by ESO treatment. Treatment with ESO, ergo, exhibits substantial neuroprotective and modulatory potentials in response to AlCl3 toxicity.
Moringa oleifera Phytochemicals Protect the Brain Against Experimental Nicotine-Induced Neurobehavioral Disturbances and Cerebellar Degeneration
(Elsevier Ltd, 2019-03) Yawson, Emmanuel
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.
Pyrethroids Exposure: Implications for Testicular Dysfunction in Rats
(2018-01) Yawson, Emmanuel
Pyrethroids are synthetic pesticides which at low dose of exposure are harmless to humans but at environmentally high concentrations they cause debilitating effects in humans and animals alike. Lack of regulation of the insecticide applications in agriculture and among Nigerian households is therefore a cause for health concern. The reproductive effects of these chemicals are not precisely known. Twenty healthy, sexually active male Wistar rats were randomly divided into four groups. Three groups were exposed to the insecticide in sprayed puffs from the aerosolized insecticide for 15, 30 and 45 seconds/day respectively in air – tight plastic housing for 60 days while one group served as the untreated control. All animals were euthanized via cervical dislocation; the testes were excised and fixed in Bouin’s fluid for routine histological studies using haematoxylin and eosin. The cauda epididymis was also excised for semen quality evaluation. Reduced body weight, alteration of testicular microstructure and significant increase in the proportion of abnormal and non-motile sperm cells were observed in animals exposed to pyrethroid. Exposure to pyrethroid insecticide may lead to body weight loss accompanied with testicular dysfunction possibly leading to sterility in the rats.

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