INTRATHECAL NORADRENALINE FACILITATES AND INHIBITS THE FLEXOR REFLEX MEDIATED BY GROUP-II AFFERENT-FIBERS VIA ALPHA-1-RECEPTOR AND ALPHA-2-RECEPTORS, RESPECTIVELY

Authors
Citation
K. Sakitama, INTRATHECAL NORADRENALINE FACILITATES AND INHIBITS THE FLEXOR REFLEX MEDIATED BY GROUP-II AFFERENT-FIBERS VIA ALPHA-1-RECEPTOR AND ALPHA-2-RECEPTORS, RESPECTIVELY, Japanese Journal of Pharmacology, 62(2), 1993, pp. 131-136
Citations number
18
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00215198
Volume
62
Issue
2
Year of publication
1993
Pages
131 - 136
Database
ISI
SICI code
0021-5198(1993)62:2<131:INFAIT>2.0.ZU;2-Q
Abstract
The effects of intrathecal noradrenaline (NA) on the flexor reflex med iated by group II afferent fibers (group II flexor reflex) were invest igated in anesthetized spinal rats. Low doses (0.01 and 0.1 mumol) of NA-HCI inhibited the group II flexor reflex, while high doses (1 and 1 0 mumol) facilitated it. In rats pretreated with the selective alpha2- antagonist yohimbine-HCI (0. 1 mumol), the effect of NA-HCI (0.1 mumol ) shifted from inhibition to facilitation. Intravenous administration of prazosin-HCI (0.1 and 1 mg/kg, i.v.), a selective alpha1-antagonist , dose-dependently antagonized the facilitation of the group II flexor reflex induced by NA-HCI in rats pretreated with yohimbine-HCI. The s elective alpha1-agonist methoxamine-HCI (I mumol) and the alpha2-agoni st clonidine-HCI (0. 1 mumol) facilitated and inhibited the group II f lexor reflex, respectively. The effects of clonidine-HCI and methoxami ne-HCI were almost the same as those of NA-HCI at doses of 0.1 and 10 mumol, respectively. NA-HCI (I and 10 mumol) and methoxamine-HCI (I mu mol) increased the spontaneous electromyogram (EMG) spikes of the musc le tibialis anterior. The time course of the increase in the spontaneo us EMG spikes was similar to that observed in the group II flexor refl ex. These results suggest that NA facilitates and inhibits the group I I flexor reflex via alpha1- and alpha2-receptors, respectively, and on e of the mechanisms of the facilitatory effects is the elevation of ex citability of the alpha-motoneuron.