Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.11.8 (FAST)
 758 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spinal cords were maintained in vitro and suction electrodes used to record activity in lumbar 4 or 5 ventral roots. Stimulation of the latero-ventral aspect of the thoracic cord elicited fast and slow responses on the same and on the opposite side of the cord. There were 5 distinct responses: ipsilaterally a short latency (d ISL), a polysynaptic and a slow response, and contralaterally a fast (d CON FAST) and a slow response. The largest amplitude component, d ISL, may arise from stimulation of propriospinal neurones; the other responses may arise from stimulation of descending pathways. The slow responses had half decay times of 13-15 s and required a high intensity stimulus to elicit a maximal response. All 5 responses were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione suggesting that kainate/AMPA receptors were involved in their generation. In addition, NMDA receptors were involved in generation of the slow responses. Potentiation of certain responses by the 5-HT2 antagonists, ketanserin, ritanserin and Lilly 53837, indicated that endogenous 5-HT was exerting a modulatory depression of these responses. In addition to eliciting the 5 responses, thoracic cord stimulation caused an inhibition of segmental reflexes evoked from the lumbar dorsal root. Exogenous 5-HT, 8-hydroxy-2-(di-n-propylamino) tetralin, 5-carboxamidotryptamine, dipropyl-5-carboxamido-tryptamine and methysergide depressed all or some of the descending responses. Blockade of adrenoceptors using yohimbine, idazoxan, prazosin or propranolol had no unequivocal effect suggesting that the release of endogenous catecholamines was minimal. Clonidine was a potent depressant of the slow responses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The pharmacology of descending responses evoked by thoracic stimulation in the neonatal rat spinal cord in vitro. 810 94

The inhibitory effects of a stimulus to the thoracic cord on lumbar segmental reflexes were investigated in the superfused cord of the neonate rat. A single stimulus to the latero-ventral cord surface at T11-T12 evoked fast and slow responses in both L4 ventral roots and inhibited rapid segmental reflexes, both ipsi- and contralaterally. The monosynaptic reflex (MSR) was strongly inhibited and the polysynaptic reflex (PSR) and contralateral fast reflex (CON FAST) were inhibited by 30-40%. The inhibition rose to a maximum 2 sec after the conditioning stimulus, plateaued between 2-20 sec and gradually waned to low levels by 100 sec. The slow segmental responses were not inhibited. Inhibition of the MSR was only elicited ipsilaterally and that of PSR was reduced by about 50% on stimulation of the contralateral thoracic cord; inhibition of CON FAST could be evoked from either side of the cord. Inhibition of the MSR from 2-50 sec was greatly reduced by 5-HT2 receptor antagonists. Ketanserin (1 microM) and ritanserin (1 microM) were equally effective but LY 53857 (1 microM) had a weaker blocking action. Only ketanserin reduced inhibition of the PSR. Prazosin (0.1 microM) did not affect inhibition of the MSR but yohimbine (1 microM) blocked it as effectively as ketanserin. This was probably due to 5-HT2 receptor blockade, since 0.1 microM yohimbine had little blocking action and 1 microM idazoxan none, nor did 0.1 microM clonidine mimic inhibition of the MSR. Inhibition of the MSR and PSR was not reduced by 1 microM naloxone, 1 microM strychnine, 1 microM bicuculline nor 10-30 microM APV. Consistent with the release of 5-HT by descending pathways, the 5-HT uptake blocker, citalopram 0.1 microM and the 5-HT releaser, p-chloroamphetamine 1 microM, depressed segmental reflexes, especially the MSR. 5-Hydroxytryptamine did not have the same depressant action on segmental reflexes as stimulation of the thoracic cord; the slow responses were most affected. Both 8-OH-DPAT (1-3 microM) and dipropyl-5-CT (1 microM) preferentially depressed the MSR. Neither spiroxatrine (0.1 microM) nor methysergide (5-10 nM) altered inhibition of the MSR. The concentration of ketanserin required to reduce sub-maximal inhibition by 50% was estimated using 2 concentrations of antagonist. The pIC50, estimated for the blockade by ketanserin of inhibition 20-50 sec after a conditioning stimulus, was 7.3-7.5. It is concluded that inhibition of the MSR and PSR does not involve mediation by glycine, GABAA nor NMDA receptors, nor release of enkephalins nor noradrenaline.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Descending inhibition in the neonate rat spinal cord is mediated by 5-hydroxytryptamine. 842 18