ABSTRACT-The effects of intrathecal noradrenaline (NA) on the flexor reflex mediated by group II afferent fibers (group II flexor reflex) were investigated in anesthetized spinal rats. Low doses (0.01 and 0.1 pmol) of NA-HC1 inhibited the group II flexor reflex, while high doses (1 and 10 imol) facilitated it. In rats pretreated with the selective a2-antagonist yohimbine-HCI (0.1 pmol), the effect of NA-HCl (0.1 tmol) shifted from inhibition to facilitation. Intravenous administration of prazosin-HC1 (0.1 and 1 mg/kg, i.v.), a selective a,-antagonist, dose-dependently antagonized the facilitation of the group II flexor reflex induced by NA-HC1 in rats pretreated with yohimbine-HC1. The selective a,-agonist methoxamine-HC1 (1 pmol) and the a2-agonist clonidine-HC1 (0.1 tmol) facilitated and inhibited the group II flexor reflex, respectively. The effects of clonidine-HC1 and methoxamine-HC1 were almost the same as those of NA-HC1 at doses of 0.1 and 10 ,umol, respectively. NA-HCI (1 and 10 pmol) and methoxamine-HC1(1 pmol) increased the spon taneous electromyogram (EMG) spikes of the muscle tibialis anterior. The time course of the increase in the spontaneous EMG spikes was similar to that observed in the group II flexor reflex. These results suggest that NA facilitates and inhibits the group II flexor reflex via a, and a2-receptors, respectively, and one of the mechanisms of the facilitatory effects is the elevation of excitability of the a-motoneuron.Keywords: Noradrenaline, a,-Adrenoceptor, a2-Adrenoceptor, Flexor reflex, Afferent fiber (Group II)Noradrenergic neurons arising from the nucleus locus coeruleus and the subjacent subcoeruleus/medial parabrachial nuclear complex innervate both the dorsal and ventral horns of the spinal cord (1 3) and exert descending effects on the flexor reflex loop. Intrathecal or intraspinal injection of noradrenaline (NA) inhibits or facilitates the nociceptive flexor reflex (4-6). As the en hancement of the nociceptive flexor reflex induced by a agonists or L-dopa, a precursor of NA, is antagonized by a-blockers (7 12), NA is considered to exert facilitatory effects via a-receptors. Although many investigations con cerning the effects of NA on the nociceptive flexor reflex evoked by noxious stimulation which can activate group IV afferent fibers (13) have been reported, there are few reports on the effects of NA on the non-nociceptive flexor reflex. The aim of this study was to investigate the effects of intrathecal administration of NA on the flexor reflex mediated by group II afferent fibers (group II flexor re flex), which is one of the non-nociceptive flexor reflexes (14), and to elucidate the functional role of a, and a2 receptors by using antagonists and agonists. MATERIALS AND METHODSMale Wistar rats (461 ± 14 g) were anesthetized with intraperitoneal injection of urethane (400 mg/kg) and a chloralose (50 mg/kg), which were supplemented as re quired. The spinal cord was transected at the level of Th 8 9 more than 2 hr prior to recording the group II flexor reflex. The gr...

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ABSTRACT-The effects of centrally acting muscle relaxants on the flexor reflex mediated by group II afferent fibers (group II flexor reflex) in anesthetized intact rats and on the intrathecal noradrenaline-HC1 induced facilitation of the group II flexor reflex in anesthetized spinal rats were investigated. In anesthetized intact rats, mephenesin, tolperisone-HCI, chlorpromazine-HC1 and baclofen inhibited the group II flexor reflex dose-dependently, whereas the inhibitory effect of tizanidine-HC1 was bell-shaped. The effect of diazepam tended to be saturated. In anesthetized spinal rats, mephenesin, tolperisone-HCI, chlorproma zine-HCI, diazepam and baclofen also depressed the group II flexor reflex, but tizanidine-HC1 slightly increased it. The intrathecal noradrenaline-HCI-induced facilitation of the group II flexor reflex was not affected by mephenesin or diazepam, but was inhibited by tizanidine-HCI, tolperisone-HCI, chlorproma zine-HCl and baclofen. These results suggest that compounds with centrally acting muscle relaxant activity depress the group II flexor reflex in different manners, and the inhibition of descending noradrenergic tonic facilitation within the spinal cord participates in the depressant action of the group II flexor reflex produced by tolperisone-HC1, tizanidine-HC1, chlorpromazine-HC1 and baclofen.

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