Cuprizone toxicity and Garcinia kola biflavonoid complex activity on hippocampal morphology and neurobehaviour.

Cuprizone-induced neurotoxicity has been employed to study the biology of remyelination in experimental models of multiple sclerosis. This study was aimed at determining the role of kolaviron, a biflavonoid from Garcinia kola, in mitigating the damaging effects of cuprizone on behaviour and the hippocampus. Twenty-four male albino mice aged 6-8 weeks were categorised into 4 equal groups: Group A (Control) received regular diet; Group B received 200 mg/kg/d of kolaviron in addition to their regular diet; Group C received 0.2% cuprizone diet only, while Group D received both kolaviron and cuprizone diet. The treatment lasted for 35 days after which behavioural tests (Morris water maze, Y maze and open field tests) were conducted and brain tissues were processed for histology, histochemistry (Nissl staining), immunohistochemistry (glial fibrillary acidic protein) and biochemistry (malondialdehyde, superoxide dismutase and glutathione peroxidase). Results showed that cuprizone toxicity led to weight loss, impairment in memory and exploratory drive, oxidative stress, chromatolysis and reactive astrocytosis; meanwhile administration of kolaviron prevented cuprizone-induced weight loss, memory decline, oxidative stress and neuromorphological alterations. In conclusion, administration of kolaviron might be useful in limiting the effects of cuprizone toxicity on the morphology and functions of the hippocampus.

Moringa oleifera Ameliorates Histomorphological Changes Associated with Cuprizone Neurotoxicity in the Hippocampal Cornu ammonis (CA) 3 Region.

Cuprizone-induced neurotoxicity has severally been used to study demyelinating diseases like multiple sclerosis(MS), adversely affecting both the white and grey matters of the brain. Lesions have been observed in different regions ofthe brain including, corpus callosum, neocortex and the hippocampal formation. The current study explored the role ofMoringa oleifera leaf extract in restoring the resultant histomorphological changes in cuprizone-induced hippocampaldamage in Wistar rats. Twenty adult female Wistar rats with average weight of 163.74 ± 3.59 g were grouped into A: Control,administered with 1 ml of normal saline, B: received 0.4% cuprizone diet, C: received 1.875 mg/ml/day of Moringa extract,and D: received a combination of cuprizone and Moringa in similar doses. Administration was oral for 5 weeks. The weightsof animals were assessed during treatment, and at the termination of experiment, the rats were euthanized and the brainswere fixed in 4% paraformaldehyde. The tissue was processed for histological and histochemical examinations using theHaematoxylin and Eosin stain and cresyl fast violet stain to assess the general microarchitecture and neuronal cellsrespectively of hippocampal cornu ammonis (CA) 3 region. The body weight of cuprizone-treated rats was reduced and thiswas ameliorated significantly in animals that were co-administered with Moringa. Similarly, there were histologicalalterations in the CA3 region of the hippocampus with the presence of pyknotic pyramidal cells organized in clusters andCA3 cells with degenerative changes, but administration of Moringa led to a better organised and fairly intact histologicalappearance. Pharmaceutical development of Moringa oleifera into appropriate therapeutic formulations could offer somerelief to patients of demyelinating conditions that have clinical features of neurological deficits.

Histological changes in the cerebelli of adult wistar rats exposed to cigarette smoke.

The different constituents of tobacco smoke have been linked to different diseased conditions. In this work, the histological effects of cigarette smoke on the cerebellum of adult male Wistar rats were studied. Sixteen Wistar rats with mean weight of 153.24 ± 4.12 g were grouped equally into four. The Control Group A was exposed to fresh air, while Groups B, C and D animals were each exposed to smoke from one, two and three sticks of cigarette respectively. Each stick of cigarette was completely consumed within an average duration of 11 minutes. Improvised smoking chambers were constructed and used for the exposure daily, while treatment lasted for 28 days. The animals were thereafter sacrificed by cervical dislocation, the cranium was exposed and the brain gently removed and weighed; the cerebellum was excised, weighed, and fixed in formol calcium, and subsequently processed for histological observation using the Haematoxylin and Eosin staining principle. Loss of weight and reduction in weight gain were noticed in the treatment groups, with corresponding reduction in cerebellar weights, in a dose-dependent pattern. Histology also revealed loss of white matter, reduction in thickness of cell layers and their cellular components. Increasing dosage of cigarette smoke could predispose to progressive compromise in the structural integrity and composition of the cerebellum, and this might result in cerebellar dysfunction.

Morphological and neurohistological changes in adolescent rats administered with nicotine during intrauterine life.

Tobacco smoking has been linked to many preventable diseases affecting various organs and systems of the body, including the brain. The current study was conducted to demonstrate the histological changes observable in the cerebral cortex of young Wistar rats exposed to nicotine during gestation. Vaginal smearing was conducted for the female Wistar rats to determine their oestrous cycle, after which they were exposed to male rats overnight, for mating. Pregnancy was confirmed and the pregnant rats were divided into 3 groups based on the 3 trimesters (A, B, C), with each group having a control and a treated subgroup. The Control Groups (A1, B1, C1) were given 0.1 ml of normal saline i. p., while the Treated Groups (A2, B2, C2) received 0.06 mg/kg/0.1 ml of nicotine intra-peritoneally. Treatment was for a period of 6 days only within each trimester for all subgroups. The pregnant animals were allowed to litter, and at postnatal day 35 they were sacrificed. The skull was dissected to expose and remove the brain; the temporal and parietal cortices were excised and fixed in 4% paraformaldehyde for histological tissue preparation, using cresyl fast violet staining techniques. Exposure of the developing brain to nicotine during gestation resulted in various degrees of abnormalities in the cytoarchitecture of the parietal and temporal cortices of young rats. The gestational period of nicotine exposure and specific cortical affectation are important factors to consider while investigating neurological abnormalities in offspring of tobacco smokers.