The Activities of the Central Nervous System Following Ethyl Acetate Extract of Mucuna pruriens Seed Administration in Male BALB/c Mice

A number of reports showed the beneficial psychotropic effects of many of the Nigerian medicinal plants, but few scientific studies have been carried out as empirical evidence. This study investigated the possible neurobehavioural effects of ethyl acetate extract of Mucuna pruriens (MP) seed in male BALB/c mice. Male BALB/c mice (2½-3 months old) were grouped into 5 (n=6), treated with normal saline (0.1 mL), n-propanol extract of MP (200, 100, 50 mg/kg) or reference drug haloperidol (HP) or diazepam (DZP); thereafter, subjected to diverse behavioural models to evaluate the central nervous system (CNS) effects of the extract. A bolus of MP (200, 100, and 50 mg/kg) decreased the rectal temperature, exploratory activities (locomotion, rearing and grooming), anxiety-like responses (% open-arms time, open-arm entries, and the total number of enclosed arms times). Additionally, a one-shot of intraperitoneal administration of MP decimated the total score of apomorphine-induced stereotyped behaviours. Latency to hexobarbitone-induced sleep increased significantly in the 200 mg/kg MP, unchanged in the 100 mg/kg MP, and decreased in the 50 mg/kg MP treated groups. There was a marked decrease in the markers of convulsion (tonic flexion, extension, clonic convulsion, stupor, and recovery time) following MP treatment, especially the higher doses (200 mg/kg and 100 mg/kg). In conclusion, the CNS effects of systemic administration of MP seed are not unrelated to its hypothermic, hypnotic, anxiolytic, and anticonvulsant effects.

Nigella sativa Oil Preserved Anxiety-Like, Motor and Memory Related Behaviours and Neuronal Integrity in Dichlorvos Induced Acetyl Cholinesterase Inhibitions in Rats

Organophosphates are irreversible cholinesterase (ChE) inhibitors with neurological consequences, and there is not yet an effective antidote. Here, we investigated the effects of Nigella sativa oil (NSO) on the ChE inhibition, neurobehavioural and histopathological changes following dichlorvos (DDVP) ingestions in rats. Thirty-two male Wistar rats were randomised into four groups, receiving 1 ml/kg of normal saline, 8.8 mg/kg of DDVP, 8.8 mg/kg of DDVP and 1 ml/kg of NSO, and 1 ml/kg of NSO only respectively, for 14 consecutive days. Locomotor, anxiety-like behaviours and spatial working memory were assessed on the 14th day, using open field (OF), Y-maze and modified elevated plus maze paradigms. The rats were euthanized on the 15th day and the brains excised; three brains were fixed for histopathology, and the other five prepared for biochemical analysis of acetyl cholinesterase (AChE). DDVP exposure caused significant reductions in frontal, amygdala and cerebella AChE activity, spontaneous alternations, line crossing and rearing frequencies and time in centre square, and caused increase in freezing period, transfer latency and necrotic-like cells. NSO intervention was able to reverse DDVP effects on AChE activities, explorative, locomotor, anxiety and spatial memory behaviours in co-exposed rats. It also preserved the histological integrity of the investigated brain regions. It can be concluded that NSO, may be potent against organophosphates induced neurotoxicity and their neurobehavioural consequences through the modulation of AChE activities.

Association of Low Visual Acuity and Head Injury among the Undergraduate Students of Bingham University, Karu, Nigeria

A laboratory-based cross-sectional study was conducted among Bingham University undergraduate students, Karu, to investigate the proportion of visual acuity (VA) among the students. The study aimed at investigating an association between head injury with low VA of students whose parent’s use medicated eye glasses. A total of 262 undergraduate students participated in the study. A predesigned, pre-tested, self-administered questionnaire was filled by the students. Eye examination using the optotype Snellen E Chart followed and the VA of the right (VARE) and left eyes (VALE) were tested separately. A regression and correlation model was used to assess the relationship between head injury and low VA. Head injury at one point of time in their life was strongly associated with low VA for both eyes (VARE, r = 0.524, R2 = 0.274, p = 0.040; VALE, r = 0.0.531, R2 = 0.282 p = 0.010). Parents’ use of medicated eye glasses was also associated with low VA of students (VARE p = 0.009; VALE p < 0.001). Our results showed that students that had any form of head injury at any point in their life either as a child, teenager or an adult, were more likely to have low VA. However, the educational status of parents, anthropometric parameters and ethnicity had no association with low VA. We conclude that any form of head injury, at any point in one’s life, and parent’s use of eye glasses are risk factors for low VA.

Investigating the Effects of Allium sativum on the Prefrontal Cortex in Lithium Chloride Pilocarpine-Induced Epilepsy in Wistar Rat

The prefrontal cortex (PFC), mediating executive brain functions is impaired in epilepsy. Allium sativum (AS) anti-seizure potential on the PFC of experimentally-induced epilepsy was investigated. Forty-eight male Wistar rats (200-250g) were randomized into six groups. Control (2mL/kg distilled water); AS only (100mg/kg); LiCl+PC (lithium chloride, 127mg/kg, and pilocarpine, 30mg/kg); LiCl+PC+AS100mg/kg and LiCl+PC+AS300mg/kg received LiCl+PC and 100mg/kg AS and 300mg/kg AS respectively; LiCl+PC+SV received LiCl+PC and sodium valproate (10mg/kg). Treatments lasted for 21 days, behavioural tests then preceded sacrifice. Brain tissues were excised, fixed in 10% neutral buffered formalin for demonstration of PFC cytoarchitecture and glial fibrillary acidic protein (GFAP) expression. Neurotransmitters were also assayed. Walling and rearing frequencies reduced significantly (p<0.05) in the LiCl+PC group compared to control. Glutamate and acetylcholine levels increased in all groups except AS only, while gamma-aminobutyric acid, dopamine, serotonin and norepinephrine levels increased in the LiCl+PC+AS100mg/kg, LiCl+PC+AS300mg/kg and LiCl+PC+SV groups compared to the control. Cytochrome C oxidase and glucose-6-phosphate dehydrogenase activities significantly increased (p<0.05) in all groups, while nitric oxide levels increased in the LiCl+PC+AS300mg/kg and LiCl+PC+SV groups compared to the control. Cytoarchitecturally, the LiCl+PC PFC showed neurodegenerative features, increased GFAP expression, while the treated groups showed preserved neurons and mild astrogliosis. Conclusively, AS showed neuroprotective potentials against LiCl+PC-induced neuronal degeneration, mitigated reactive PFC astrogliosis. However, AS did not lower glutamate and other neurotransmitter levels.

Ascorbic Acid Supplementation Attenuates Hippocampal Neuronal Damage in Orchiectomized Rats

Understanding the bidirectional relationship in the cellular and molecular mechanisms associated with testosterone deprivation and cognitive activities has become a high-priority goal. Testosterone has been shown to have effects in the nervous system, ranging from targeting gene expression to modulating neurotransmission. This study therefore evaluated the modulatory role of ascorbic acid in the hippocampus of orchiectomized rats. Twenty-one adult male Wistar rats with an average weight of 170g±10g were randomly assigned into three groups of seven rats each; the control, orchiectomized (orchiectomy+flutamide, 11 mg/kg body weight, bw), and ascorbic acid (orchiectomy+flutamide, 11 mg/kg bw + ascorbic acid, 100 mg/kg bw). Treatment was by oral gavage and lasted for 30 days. Nitrosative stress and neuroinflammatory analysis, hormonal, histological and immunohistochemical expression of astrocytes in the hippocampus were examined. Results showed significantly increased expression of acetylcholinesterase, inducible nitric oxide synthase, and tumour necrotic factor-alpha in the hippocampus of orchiectomized animals. There was altered cytoarchitectural morphology evidenced by reduced Nissl profiles in neuronal axons and dendrites, which corresponded to apoptotic changes, and increased expression of reactive astrocytes suggesting neuronal damage. Nitrosative stress and inflammatory perturbations were well modulated in animals treated with ascorbic acid with unaltered hippocampal morphology. The results indicated that decline in brain androgen activities caused inflammatory and oxidative stress-driven alterations in the hippocampus, while ascorbic acid supplementation offered therapeutic value by modulating neurochemicals and scavenging free radicals in the hippocampus.

Neurocognitive and Neuroarchitectural Changes in the Prefrontal Cortex of Wistar Rats Treated with Highly Active Antiretroviral Therapy

The use of highly active antiretroviral therapy has proven to be highly effective in the treatment of human immunodeficiency virus 1 (HIV-1) infection. However, its impact on cognition has not been fully explored. This study was designed to assess the impacts of antiretroviral therapy on cognitive function and histoarchitecture of the prefrontal cortex of Wistar rats. Forty adult male Wistar rats weighing 180-200 g were randomly assigned to 4 groups: control, tenofovir, lamivudine and efavirenz (n=10), which received 1 ml distilled water and 6 mg/kg, 6 mg/kg and 12 mg/kg, respectively. Spatial memory scores were assessed using the Y-maze test. Following behavioural studies, the animals were euthanized, and their whole brains harvested. The prefrontal cortex was sectioned and processed for oxidative stress, histological and immunohistochemical analyses. There was a significant decrease in percentage alternation evaluated from the right/wrong decisions scored from the tenofovir and lamivudine groups, compared to the control group (p<0.05). malondialdehyde (MDA) and reduced glutathione (GSH) levels were elevated following lamivudine and tenofovir exposure in the rats’ prefrontal cortices, respectively, compared to control (p<0.05). There were also significant alterations of cortical pyramidal cells in the tenofovir and lamivudine groups. Additionally, marked astrogliosis with increased glial fibrillary acidic protein expression was observed, consistent with the structural alterations, especially in the lamivudine group. Our findings suggest that, of the three highly active antiretroviral therapy (HAART) drugs studied, lamivudine may be a major culprit in the progressive neurological damage and cognitive impairment in HIV-infected individuals on HAART.

Chronic Administration of Combined Oral Contraceptive Pill Causes Prefrontal Cortical Oxidative Stress in Female Wistar Rats

Combined oral contraceptive pill (COCP) is used by women to prevent ovulation. This study investigated toxicological effects of COCP on the brain of female rats. Fifteen rats were divided at random into three groups (n=5): Normal control, and first and second cycles treated orally with COCP (0.04 μg/kg bwt of ethinyl oestradiol and 2 μg/kg bwt levonorgestrel) daily for 21 and 42 days respectively. Toxicological effect of treatment on the brain was assessed in the prefrontal cortical acetylcholinesterase, sodium/potassium-ATPase (Na+/K+-ATPase), superoxide dismutase and catalase activities, lipid peroxidation and reduced glutathione levels. Histomorphological examination of the prefrontal cortex of the rats in all the groups was carried out. Activities of cortical Na+/K+-ATPase, acetylcholinesterase, superoxide dismutase and catalase were significantly (p<0.05) reduced following chronic administration of COCP. Histomorphological study of the pre-frontal cortex showed large pyramidal neurons, pyknotic pyramidal neurons, condensed nuclei and increased perineural spaces. Results showed that chronic administration of oral contraceptive caused prefrontal cortical oxidative stress by repressing activities of antioxidant enzymes, Na+/K+-ATPase and acetylcholinesterase.

Tetrapleura tetraptera (Schumach.) Taub. Fruit Extract Improves Cognitive Behaviour and Some Brain Areas of Pentylenetetrazol-Kindling Rats

Epilepsy is a neuronal disorder that arises from imbalances of some neurotransmitters and manifests as recurrent seizure and cognitive impairment. Most antiepileptic drugs are either expensive, not effec¬tive or are associated with adverse effects warranting efficacious alternatives. This study, therefore, investigated the activity of Tetrapleura tetraptera (Schumach.) Taub fruit extract (TTE) on the behaviour and some brain areas of pentylenetetrazol (PTZ)-kindling rats. Thirty-five male Wistar rats (150-200 g) were assigned into five groups (1-5, n=7): Control (distilled water); TTE (500 mg/kg); PTZ (40 mg/kg); PTZ (40 mg/kg) pre-treated with either sodium valproate (SV, 200 mg/kg) or TTE (500 mg/kg). All treatments were oral, except for the PTZ (intraperitoneally), and carried out 48 hourly, until kindling was also fully achieved (21 days). Subsequently, there was a beam walking behavioural test, deep anaes-thesia and animals’ sacrifice, while whole brains were processed for histology. The results showed that seizure was induced with higher mortality in the PTZ group, and was suppressed with higher quantal protection in the PTZ groups pre-treated with either TTE or SV. There was no difference (p>0.05) in beam walk slips and latency. Simultaneously, the PTZ group showed some degenerative cellular changes in the hippocampus and temporal cortex, with significantly (p<0.05) higher cellular density, except in the cerebellum. These cellular changes were either minimal or not apparent in the PTZ groups pre-treated with either TTE or SV compared with the control group. In conclusion, TTE protected against PTZ - induced seizures and brain histopathology of rats, with results similar to the standard anticonvulsant drug, SV.

Rodent Experimental Model of Konzo: Characterization of Motor Impairment and Neurodegeneration after Cassava Neurotoxicity in the Rat

Konzo is a motor neuron neurodegenerative disease caused by bitter cassava toxicity that presents as a non-progressive spastic paraparesis. The ability of bitter cassava to produce behavioural and structural changes in adult rat nervous system was examined. Twenty five rats were used for this study, and pruned to 20 after consistent baseline performance was achieved (n=20; control=5, cassava chow=15). The rats were switched to a cassava diet for another 5 weeks (n=15). After the cassava consumption period, 5 rats underwent rehabilitation training three times a week and their performance tested once in a week for 5 weeks. Quantitative and qualitative assessments using a reaching movement scale and reach-to-grasp success rate were respectively carried out. Animals subjected to cassava toxicity performed significantly worse than the controls when determining the success rate in a reach-to-grasp experiment (baseline=69.8%, cassava diet=21.4%, post-cassava diet =48.9%). The various movement of the rat was analysed using ANOVA and there was significant difference (p < 0.05) in the performance. The rats couldn’t pronate, grasp, withdraw or open the digits properly when fed with cassava diet. Histology showed neuropathological damages on the motor cortex, less neurons in the motor neuron pool of the spinal cord and disruption of pyramidal layer of the hippocampus when rats were given bitter cassava. Immunofluorescence stain shows motor neurons and numerous choline acetyltransferase (ChAT+) processes and some C-boutons. There are behavioural evidence and neuropathological changes in the motor cortex and ventral horn of the spinal cord that may underlie movement impairments in rats fed with bitter cassava.

Influence of Antidepressant Medication on Short Term Memory in Chronic Mild Stress Mouse Model of Depression

Depression is among the most prevalent diseases worldwide. Researchers have identified a link between depression and different types of memory loss, including short term memory (STM). Also, the memory impairment in depression is a function of severity. This study was conducted to evaluate the effect of antidepressant medication on short term memory in chronic mild stress (CMS) mouse model of depression. A total of eighteen female mice were randomly divided into three groups of six mice each (n=6). Group I served as normal control, group II were exposed to CMS for 14 days, group III were exposed to CMS for 14 days, and thereafter treated with paroxetine at a dose of 20 mg/kg for 14 days. Short term memory was assessed using batteries of cognitive tests including the Y-maze and novel object recognition. Further antidepressant effect was measured using the tail suspension test (TST). The results showed that paroxetine at 20 mg/kg significantly improved the short term memory of the depressed female mice (p<0.05) in the Y-maze and novel object (recognition) tasks after CMS. Therefore, paroxetine might be used to enhance short term memory in depressed individuals, although clinical studies are required to confirm this finding.