Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was undertaken on the effects of kainic acid lesioning on the nodulus of the rat cerebellum on behavior and various brain receptors in conscious, freely moving rats. The basis for the study was the observation that barrel rotation and other motor effects induced by intraventricular administration of vasopressin and nicotine could be elicited by their administration into the nodular area of the cerebellum. Histology revealed a marked destruction of Purkinje, stellate, and Golgi cells in the area surrounding the site of kainate administration, with little effect on the granular cells. Immediately after administering 4-12 ng of kainic acid into the nodular cerebellum, rats exhibited circling movements, barrel rotation, and clonic convulsions accompanied by stereotypic head movements, aggressiveness, and gnawing-biting; effects gradually diminishing over 3 days. Receptor binding studies 4-14 days after kainate lesioning revealed a marked increase in 3H-nicotine and 3H-QNB binding in the surrounding cerebellar region, caudate nucleus, and hypothalamus, with no change in 3H-dihydromorphine binding. The findings are consistent with the hypothesis that nicotinic and muscarinic pathways in the vestibular cerebellum, along with its connection to nigrostriatal dopaminergic systems, are involved in the mediation of barrel rotation, ataxia, and other motor disturbances resulting from administration of vasopressin on nicotine intraventricularly.
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PMID:Behavior and receptor changes after kainate lesioning of nodular cerebellum. 302 7

Canine Inherited Ataxia (CIA) is an autosomal recessive cerebellar disease of Gordon Setters associated with degeneration of Purkinje and granule cells. To define specific biochemical correlates of neuronal loss, synaptic neurochemical parameters were measured in three cerebellar regions (vermis, "pars intermedia," and hemisphere) at early and late stages of this disease. At one and a half years of age, affected dogs showed the most severe lesions in the "pars intermedia," with a 39% decrease in the number of Purkinje cells and a 29% decrease in granule cells. Neurochemical measurements demonstrated decreased [3H]muscimol binding and elevations in norepinephrine concentration (248% above control) and [3H]glutamate receptor binding (118% above control). At five years of age, reduction of Purkinje cells in the three cerebellar regions ranged from 65 to 91% while loss of granule cells was between 13 and 53%. [3H]Muscimol binding remained low throughout the cerebellum (38 to 59% of control) and norepinephrine concentration and [3H]glutamate binding were markedly reduced from the levels observed at one and a half years. Glutamate decarboxylase activity, [3H]QNB binding and GABA concentration were relatively unaffected. Our results indicate that neurochemical parameters associated with cerebellar neuronal systems demonstrate specific alterations in a chronic degenerative disorder. This study also indicates the importance of evaluating neurochemical measurements with regard to both spared and degenerating neuronal systems and emphasizes the role of compensatory neurochemical alterations in cerebellar degenerative disorders.
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PMID:Synaptic neurochemical alterations associated with neuronal degeneration in an inherited cerebellar ataxia of Gordon Setters. 650 89