Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Wet-dog-shaking resembling morphine withdrawal behaviour can be evoked in rats by administration of dipropylacetate (DPA). It has been postulated that DPA elicits the withdrawal like behaviour through specifically inhibiting the GABA-degradation in nerve terminals. Inhibition of GABA-transaminase (GABA-T) by aminooxyacetic acid (AOAA) in other compartments of the brain would result in an inhibition of the stimulated GABA-release via feedback on autoreceptors and therefore suppress the DPA-evoked behaviour. This hypothesis has been tested using the GABA-T inhibitors gamma-acetylenic-GABA (GAG), gamma-vinyl-GABA (GVG) and ethanolamine-O-sulphate (EOS). Although GAG and AOAA were found to suppress the body shakes, both GVG and EOS had no effect. Both GAG and AOAA have possibly also effect on glutamate decarboxylase (GAD) whereas GVG and EOS did not affect this enzyme, suggesting a nerve terminal-specific effect on DPA-induced behaviour. GVG stimulated DPA-evoked body shakes after 36 and 60 h, when a specific GABA-increase in nerve terminals will be present.
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PMID:Quasi-morphine withdrawal behaviour: indication for a specific involvement of the GABA-ergic nerve terminal compartment. 642 Jun 29

The reticular thalamic nucleus consists of densely packed neurons containing the neurotransmitter GABA. It surrounds the lateral border of the thalamus, has extensive reciprocal connections with thalamocortical neurons, and is thought to be involved in attentional processes. The reticular thalamic nucleus also receives direct and indirect inputs from the basal ganglia, suggesting that it may be involved in relaying motor information to the thalamus and cortex. We examined the possibility that decreased dopaminergic transmission in the basal ganglia indirectly affects the reticular thalamic nucleus. Rats received unilateral 6-hydroxydopamine lesions of the substantia nigra pars compacta and were killed two or three weeks after the lesion. Sections of the reticular thalamic nucleus were processed for in situ hybridization histochemistry at the single cell level with RNA probes for both isoforms of glutamate decarboxylase (M(r) 65,000: glutamate decarboxylase 65 and M(r) 67,000: glutamate decarboxylase 67), the rate limiting enzyme of GABA synthesis. Unilateral nigrostriatal dopaminergic lesions induced a topographically specific, bilateral increase in glutamate decarboxylase 67 messenger RNA in neurons of the lateral and ventral reticular thalamic nucleus. A much smaller increase in glutamate decarboxylase 65 messenger RNA was observed which was significant only ipsilateral to the lesion. Short- (seven day) and long-term (eight month) treatments with the antipsychotic drug haloperidol, in regimens that preferentially block D2 dopamine receptors, induced catalepsy and orofacial dyskinesia, respectively, but did not alter glutamate decarboxylase 67 messenger RNA levels in the reticular thalamic nucleus. Thus, loss of dopaminergic terminals, but not blockade of D2 dopamine receptors, induced the effects observed in the reticular thalamic nucleus. The results reveal a novel bilateral effect of unilateral dopamine depletion. In view of the role of the reticular thalamic nucleus in tremor and attentional processes, which are altered in Parkinson's disease, this effect may contribute to the clinical manifestations of nigrostriatal dopamine depletion.
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PMID:Unilateral nigrostriatal lesions induce a bilateral increase in glutamate decarboxylase messenger RNA in the reticular thalamic nucleus. 905 94