Cerebellum Of Wistar Rats Research Articles

Effect Of Artesunate On The Nissl Bodies Of The Cerebellum Of Wistar Rats

The study was to assess the effect of the administration of different doses of artesunate on the Nissl bodies of the cerebellum of Wistar rats. Twenty adult albino Wistar rats weighing between 160-180g were equally assigned into four groups (A, B, C and D). Group A served as the control that received distilled water, while groups B, C and D were the experimental groups. Groups B and C received 2.86mg/kg and 5.71mg/kg of artesunate respectively for three days, while group D received 2.86mg/kg of artesunate for six days. Twelve hours after the last administration the animals were sacrificed. There was reduced staining intensity of Nissl bodies in groups B, C and D compared to the control. The reduction in staining was more in groups C and D especially in the granular and Purkinje cortical layers. These results revealed that artesunate cause reduced Nissl bodies of the cerebellum of Wistar rats, and these reductions were dose and time dependent.

The Effect Of Larimal® Administration On Nissl Substances Distribution In The Cerebellum Of Wistar Rats

Larimal® is an artemisinin base antimalarial drug made up of amodiaquine and artesunate. Thus the effect of this drug on Nissl substances distribution in the cerebellum of Wistar rats was carried out. Twenty adult Wistar rats were divided equally into four groups. Group 1 served as the control and the animals received distilled water, while groups 2, 3 and 4 were the experimental groups and the animals were treated with 17.50mg/kg+5.71mg/kg, 8.75mg/kg+2.86mg/kg and 8.75mg/kg+2.86mg/kg of Larimal® respectively. The administration lasted three days for groups 2 and 3, and six days of group 4. Nissl substances staining were reduced in groups 2 and 4 compared to groups 1 and 3. Thisindicates chromatolysis in groups 2 and 4, a result of tissue toxicity. This result reveals that increase dose and duration of Larimal® is toxic to cerebellar tissues which may likely result in cerebellar dysfunction.

NCS-1 Expression in Rat Brain after Electroconvulsive Stimulation

Although electroconvulsive therapy (ECT) has been used as a treatment for mental disorder since 1930s, little progress has been made towards understanding the mechanisms underlying its therapeutic and adverse effects. The aim of this work was to analyze the expression of NCS-1 (neuronal calcium sensor 1, a protein that was found to be altered in post-mortem prefrontal cortex of schizophrenic patients) in striatum, cortex, hippocampus and cerebellum of Wistar rats after acute or chronic electroconvulsive stimulation (ECS). Rats were submitted to a single stimulation (acute) or to a series of eight stimulations, applied one every 48 h (chronic). Animals were killed for collection of tissue samples at time zero, 30 min, 3, 12, 24 and 48 h after stimulation in the acute model and at the same time intervals after the last stimulation in the chronic model. Our results indicated that chronic ECS increased the expression of NCS-1 only in cerebellum. Such results on the expression of proteins involved in signaling pathways that are relevant for neuropsychiatric disorders and treatment, in particular ECT, can contribute to shed light on the mechanisms related to therapeutic and adverse effects.

Effects of noradrenaline depletion on adrenergic and muscarinic cholinergic receptors in the cerebral cortex, hippocampus, and cerebellum

The effects of noradrenaline depletion on α- and β-adrenergic and muscarinic cholinergic receptors in the cerebral cortex, hippocampus, and cerebellum of Wistar rats were studied. Noradrenaline depletion was obtained either by chemical (6-hydroxydopamine) lesions of the locus cerulet's or by chronic reserpine treatment. Two weeks after locus ceruleus lesions and 10 days after chronic reserpine treatment, the rats were killed and the cerebral cortex, hippocampus, and cerebellum dissected. A small portion of each tissue was assayed for noradrenaline, to assess the success of locus ceruleus lesions or reserpine treatment, and the remainder was used to measure the specific binding of tritiated α- and β-adrenergic and muscarinic cholinergic receptor ligands to particulate fractions of these tissues. The effect of noradrenaline depletion on isoproterenol-induced cyclic AMP generation in cerebellar slices was also studied. Noradrenaline depletion whether by locus ceruleus lesion or chronic reserpine treatment induced reproducible and significant increases in the binding to β-adrenergic receptors in the cerebral cortex and hippocampus. Scatchard analyses revealed that this increased binding was due to an increased density of β-adrenergic receptor binding sites. In the cerebellum, however, noradrenaline depletion did not result in an increase in β-adrenergic receptor binding nor in isoproterenol-induced cyclic AMP generation. Noradrenaline depletion did not cause significant changes in the binding characteristics of α-adrenergic or muscarinic cholinergic receptors in any of the three regions of the brain that were studied.

Content and composition of the gangliosides of forebrain, brain stem and cerebellum of the rat during normal and restricted growth.

The effect of undernutrition was studied on the content and composition of the gangliosides of forebrain, brain stem, and cerebellum of Wistar rats. Undernourishment from before birth upto 21 days of age did not produce any significant change in the content of gangliosides in any brain area, but when continued upto 121 days it resulted in a significant decrease of the lipids in each of these brain regions. At this age the different ganglioside fractions were, however, affected differently in the different brain areas. Thus the accumulation of the ganglioside GD1a was most affected in the forebrain, of ganglioside GD1b in the brain stem, and of ganglioside GT1 in the cerebellum. These were the largest fractions of total gangliosides in the respective brain areas at 121 days of age. The results suggest that the brain may be vulnerable to undernourishment at any time when a biochemical process in development of the tissue is in progress.

Heterotopic cell nests in the developing rat cerebellum.

Serial sagittal sections of the postnatally developing cerebellum of Wistar rats were studied to determine the incidence, origin, and relation to other cerebellar structures of nests of heterotopic cells. These nests were found to consist of small, darkly staining cells of either irregular or elongate shape with large, dark nuclei and bore close resemblance to cells of the external granular layer. They were present in every animal from the day of birth to at least day 15 of life and were confined to the uvula, nodulus, and pyramis of the vermis. In addition, the cell nests were found to be perivascular and continuous with the external granular layer via a narrow tongue of cells surrounding capillaries which penetrated to the medullary layer of the cerebellum from the subarachnoid space. The significance of the nests in relation to other studies, and their involution after day 15 of life is briefly considered.