Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1 The effect of catechol on uptake and K+-stimulated release of gamma-aminobutyric acid (GABA), D-aspartate, noradrenaline and acetylcholine has been studied in slices of cerebral cortex and thalamus. 2 Low concentrations of catechol did not influence the uptake of any of the neurotransmitters in either brain area. 3 Noradrenaline release was unaffected by catechol. 4 Acetylcholine release from both cortical and thalamic slices was inhibited by high concentrations of catechol. This phenomenon is unlikely to be related to catechol-induced convulsions. 5 Catechol (100 microM) inhibited GABA release from cortical slices by 28%. However, at a concentration of 10 microM catechol enhanced the release of D-aspartate from thalamic slices by over 100%. 6 Potentiated release of excitatory amino acid transmitters may contribute to the enhanced excitability of thalamic cells which occurs during sensory myoclonus induced by low doses of catechol.
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PMID:The effect of the convulsant agent, catechol, on neurotransmitter uptake and release in rat brain slices. 611 45

Catechol- and urea-induced myoclonus models in the rat were electrophysiologically compared to clarify pathophysiological differences. Catechol-induced myoclonus had various similarities with cortical reflex myoclonus in that there were electroencephalogram (EEG) discharges prior to myoclonic discharges, a spread of myoclonic discharges from the rostral to the caudal site, and a high amplitude somatosensory evoked potential (SEP). In urea-induced myoclonus, there were no EEG discharges related to myoclonic discharges and no enlarged SEP components as in reticular reflex myoclonus. Catechol-induced myoclonus had two evoked EMG responses of the biceps femoris at mean onsets of 8.0(C1) and 13.4 (C2) ms, and urea-induced myoclonus had a response (U1) at the mean onset of 10.2 ms. A study of the effects of various lesions in the central nervous system on these evoked EMG responses suggests that C1 is a monosynaptic spinal reflex. C2 which disappeared when the bilateral sensorimotor cortex for the hind limb had been resected and the lesion cooled is generated by the deep cerebral structures, such as the thalamus or basal ganglia, and U1 originates in the brain stem reticular formation. These results imply definitive differences of the pathophysiological mechanisms between catechol- and urea-induced myoclonus.
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PMID:Electrophysiological comparison between catechol- and urea-induced myoclonus models in the rat. 840 42