Atropine exposure in adolescence predispose to adult memory loss in Wistar rats

Some of the brain malfunctions in adulthoods have been linked to the developmental process in their childhood, especially in most adolescent who have been exposed to one form of drug abuse or another. This study investigated the effect of atropine exposure at adolescence on the memory and histology of the frontal cortex of Wistar rats and its effects on adult memory. 20 male adolescent Wistar rats were used for the study. The rats were divided into two groups of 10 rats each. The first group were administered with100 mg/kg body weight of atropine (Atr), and the other 10 rats were given 10 mL/kg body weight of normal saline (NS) for 7 days at adolescence. On 8th day, the rats were subjected to novel object recognition test (NOR) and ‘Y’ maze test to assess their memory function, 5 rats from each group were euthanized using ketamine and were perfused transcardially with 4% paraformaldehyde. Thereafter, the brains were removed and processed for histology using H&E and Giemsa stain. The remaining 5 rats from each group were reared till adult (65 days postpartum) without treatment denoted as Atr-I and NS-I respectively. The same memory tests and histology study were conducted on the rats at adulthood. Data were analysed using Student t test and P<0.05 was set as significant level. Atr and Atr-1showed decline in memory neither index from NOR compared with NS and NS-I respectively. Atr-I shows decline in Y maze compared to NS-I. The study concludes that atropine exposed rats show significant signs of neural cell death in the frontal cortex which progresses into adulthood as evidence from the histological findings

Alcohol-pentazocine combination: implication on the cytoarchitectural profile of the medial prefrontal cortex and cerebellum of juvenile male rats

Recently, Pentazocine and alcohol have become one of the drugs abused in the developing countries. However, there is the dearth of information on the effects of these substances on the cytological profile of the medial prefrontal cortex (mPFC) and cerebellar cortex; hence this study was aimed at evaluating the effect of these substances on the cytoarchitectural profile of the mPFC and cerebellar cortex of juvenile male rats. Twenty-four juvenile male rats were used for this study. They were randomly assigned to control (A), Alcohol-treated (B), Pentazocine-treated (C), and Pentazocine-Alcohol-treated group (D). Exposure to the various treatment paradigm was done s.c. twice daily (6hrs interval) for 14 days. It was observed that the cytological profile of the mPFC of the rats in the control groups was visible and well defined. In the B, C and D groups, there were numerous forms of neurodegeneration. There was also an increase in the density of astrocytes with the presence of glial scars. Furthermore, features of degenerative changes were also seen in the cerebellar cortex of the rats in the B, C, and D groups. It was observed from this study that exposure to Pentazocine-Alcohol combination triggers inflammatory and neurodegenerative processes in the cytoarchitectural profile of the mPFC and cerebellar cortex in juvenile male rats. These features could impair the functional integrity associated with these brain regions.Keywords: addiction, substance abuse, opioid, male, youn

Activation of pro-apoptotic cells, reactive astrogliosis and hyperphosphorylation of tau protein in trimethyltin-induced hippocampal injury in rats

Neurodegenerative diseases cause neural cells to lose both the functional and sensory abilities as a result of genetic factors, proteopathies and mitochondrial dysfunction. Neurodegeneration forms the basis of most neurodegenerative disorders for example Alzheimer’s disease, Huntington’s diseases, and Parkinson’s diseases. The mechanism that underlines the process of neurodegeneration is not well understood. Understanding the process and mechanism involved in neurodegeneration might offer a better therapeutic approach to positively manage cases of neurodegenerative diseases. Therefore, this study’s target was to create an animal model to study neurodegeneration. Sixteen adult male Wistar rats were used in the study and divided into two groups. Control (0.2 mL of normal saline (NS)), and trimethyltin-treated (TMT, 8 mg/kg stat dose only). These animals underwent perfusion with 4% paraformaldehyde, brain excision and analysis of p53 antigen, GFAP and Bielshowsky on these tissues. The results showed that animals in the control group showed presence of activated p53 antigen, reactive astrogliosis, neurofibrillary tangles, and amyloid plaques within the cytoplasm of the hippocampal cells. Cornus Ammonis (CA2) and (CA3) showed more of the trimethylrtin injury than CA1 and CA4. This study thus revealed that, intra-peritoneal administration of single dose of 8mg/kg of trimethyltin can offer an attractive disease model to study some neurodegenerative diseases. Keywords: p53 antigen, Bielshowsky, Glia fibrillary acidic protein, Trimethyltin, Hippocampus

Dichlorvos induced oxidative and neuronal responses in rats: mitigative efficacy of Nigella sativa (Black Cumin)

Summary: Poisoning from Organophosphates (OPs), especially Dichlorvos (DDVP) has become endemic due to the increasing use in house hold and agricultural pests control, with most marked effects in the nervous system. However, it is evidenced that natural antioxidants are efficacious against OPs toxicity. Thus, this study investigated the possible antidotal efficacy of Nigella sativa oil (NSO) in Dichlovos (DDVP) induced oxidative and neuronal damages in Wistar rats. DDVP was administered at sub-chronic daily dosage of 8.8 mg/kg.bw for 7 days and a post-administration of NSO at 1 ml/kg.bw for the subsequent 7 days. The rats were euthanized on the 15th day, blood sample collected via cardiac puncture, centrifuged and the plasma used for biochemical analysis of total antioxidant capacity (TAC), reduced glutathione (GSH) and total reactive oxygen species (ROS), while the frontal, occipital and cerebellar cortices and the medulla were removed for histo-morphological examinations. The results showed significant (P≤0.05) decrease in plasma TAC and GSH, while a significant (P≤0.05) increase in ROS was recorded, and some vacuolation around the neurons especially in the frontal and cerebellar cortices following DDVP exposure. However, post treatment with NSO was observed to be efficacious in the recovery of the oxidative activities and the neuro-architectural integrities. Thus, it can be concluded that the antioxidant capacity of NSO could be efficacious against OPs induced oxidative damages, especially in dichlorvos accidents.Keywords: Organophosphates, antioxidant capacity, antidote, Nigella sativa oil, neurotoxicity, poisonin

Memory, neurogenic protein and oxidative deficits of frontal cortex following chlorpyrifos/dichlorvos exposure in rats

Objective: The use of xenobiotics to boost agricultural productivity has led to toxic chemicals exposure including organophosphates, causing adverse health outcomes including behavioral and neuronal impairments. This study aimed to evaluate the memory indices, possible oxidative and cholinesterase outturnson the frontal cortices of rats exposed to organophosphates.Methodology: Thirty-two Wistar rats were grouped into four. They received 1ml/kg of Normal, 8.8 mg/kg dichlorvos, 14.9 mg/kg chlopyrifos, and 8.8 mg/kg dichlorvos plus 14.9mg/kg chlorpyrifos respectively. They had training trials in the Y Maze paradigm then spatial working memory assessment. They were euthanized 24hours following exposure and tissues excised for analysis.Results: A marked reduction in metabolic markers, Acetylcholine Esterase (AChE) activity, spatial memory indices and proliferative neuron marker (Ki67) were observed. Also, increase in oxidative stress markers in the frontal cortices of the organophosphates exposed rats.Conclusion: The findings demonstrated neurotoxic effects of organophosphates in rats

Haematological effects of aqueous extract of Vernonia amygdalina and a known immunostimulant In Wistar Rats

Plants have provided sources of drugs which have made contribution to health. The use of plant extracts for the treatment of diseases is being practiced widely. Vernonia amygdalina (VA), otherwise known as bitter leaf is a shrub that grows commonly in tropical Africa and consumed as vegetable. People have considered bitter leaf as a traditional medicine, as its being used for the treatment of various illnesses such as fever, diarrhea, malaria, etc. However, its haematological effects are to be explored in this study.Thirty adult male wistar rats weighing averagely 150g were studied. They were housed, fed and cared under humane conditions in the animal house. They were divided into six groups of 5 each, with groups I and II being controls while the others were experimental. Prednisone was administered for two weeks, then blood samples were taken following which the treatments were given for specified periods. The animals were thereafter sacrificed and blood samples for CD4 and haematologic parameters taken, as well as splenic organ for histology.The results show weight increase across all groups. There was no appreciable difference in the CD4 and red blood cell count in the bitter leaf groups while the levamisole had significant decrease in these parameters. Bitter leaf was associated with significant decrease in haemoglobin level. The photomicrographs of the spleen showed decrease dimension in the white pulp and marginal zone. Levamisole and Vernonia amygdalina were associated with decreased haematological parameters.Keyowrds: Vernonia amygdalina, Levamisole, Haematological parameters, Wistar rat

Repeated acute oral exposure to cannabis sativa impaired neurocognitive behaviours and cortico-hippocampal architectonics in wistar rats

The most abused illicit drug in both the developing and the developed world is Cannabis disposing users to varying forms of personality disorders. However, the effects of cannabis on cortico-hippocampal architecture and cognitive behaviours still remain elusive. The present study investigated the neuro-cognitive implications of oral cannabis use in rats. Eighteen adult Wistar rats were randomly grouped to three. Saline was administered to the control rats, cannabis (20 mg/kg) to the experimental group I, while Scopolamine (1 mg/kg. ip) was administered to the last group as a standard measure for the cannabis induced cognitive impairment. All treatments lasted for seven consecutive days. Open Field Test (OFT) was used to assess locomotor activities, Elevated Plus Maze (EPM) for anxiety-like behaviour, and Y maze paradigm for spatial memory and data subjected to ANOVA and T test respectively. Thereafter, rats were sacrificed and brains removed for   histopathological studies. Cannabis significantly reduced rearing frequencies in the OFT and EPM, and increased freezing period in the OFT. It also reduced percentage alternation similar to scopolamine in the Y maze, and these effects were coupled with alterations in the cortico-hippocampal neuronal architectures. These results point to the detrimental impacts of cannabis on cortico-hippocampal neuronal architecture and morphology, and consequently cognitive deficits.Keywords: Anxiety, Cannabis toxicity, Cortex, Memory, Hippocampu

Black seed oil ameliorated scopolamine-induced memory dysfunction and cortico-hippocampal neural alterations in male Wistar rats

This study was conducted to evaluate cognitive enhancing effect and ameliorative effects of black seed oil in scopolamine induced rat model of cognitive impairment. These effects were investigated on scopolamine-induced dementia model in Morris water maze test (MWM) and Y maze test. The hippocampal histoarchitectural responses to scopolamine and Nigella sativa oil were also examined. Scopolamine (1 mg/kg ip) was given to induce dementia, followed by oral administration of BSO (1 ml/kg) for 14 consecutive days. MWM and Y-maze paradigms were used to assess hippocampal and frontal dependent memory respectively, thereafter the rats were sacrificed and brains were removed for histopathologic studies. Scopolamine resulted in memory impairment, by delayed latency in the MWM, reduced percentage alternation in the Y maze that was coupled by alterations in the cortico-hippocampal neurons. Posttreatment of rats with BSO mitigated scopolamine-induced amnesia, by reducing latency period and increasing percentage alternation and histological changes. The observed anti-amnestic effect of BSO makes it a promising anti-amnesic agent for clinical trials in patients with cognitive impairment

Datumetine Preferentially Upregulates NMDAR Signalling Pathways in Different Brain Regions of Mice

Introduction: We previously reported that datumetine possesses binding affinity with N-methyl-D-aspartate receptor (NMDAR) and that 14-day exposure to datumetine altered NMDAR signaling by mimicking glutamate toxicity. Here, we investigated the potential neuroprotective effect of a single shot of a low dose of datumetine administration in BALB/c mice.Methods: 30 male adult BALB/c mice were used for the study. The mice were randomly divided into three groups of ten mice each with an intraperitoneal injection of 0.1 mL of 10% DMSO for the Vehicle group, Datumetine group were administered 0.1 mg/kg body weight (bw) of datumetine and MK-801+Datumetine group were administered 0.5 mg/kg bw of MK-801 (to block NMDAR) followed by 0.1 mg/kg bw of datumetine after 30 minutes. 24 hours after administration, mice were euthanized in an isoflurane chamber followed by perfusion with 1X PBS. Brains were excised and stored at -200C till further processing. Mice designated for IHC were further perfused with 4% PFA and brain excised and stored in 4% PFA till further processing. NMDAR signalling molecules expression was evaluated in frozen brain samples and the fixed brain samples were stained for neuron, vGlut and NMDAR subtypes.Results: Relative to vehicle (Veh), datumetine downregulate calcium calmodulin kinase II alpha (CamKIIα) expression in the hippocampus and prefrontal cortex (PFC) but not in the cerebellum, cyclic AMP response element binding protein (CREB) was also upregulated only in the PFC but phosphorylated CREB (pCREB) was also upregulated in three brain regions observed, while brain-derived neurotrophic factor (BDNF) was only upregulated in hippocampus and PFC of Datumetine relative to vehicle (Veh). On the other hand, dizocilpine (MK-801) reversed some of the effects of datumetine in the observed brain regions. No major histological alterations were observed in the different brain regions immunohistochemically.Conclusion: We conclude that a low dose of datumetine moderately enhances NMDAR activity. This showed the neuroprotective potentials of low datumetine exposure