CAN THE ALPHA(2)-ADRENOCEPTOR AGONIST-MEDIATED SUPPRESSION OF NOCIFENSIVE REFLEX RESPONSES BE DUE TO ACTION ON MOTONEURONS OR PERIPHERAL NOCICEPTORS

To exclude the possibility that the suppression of nocifensive reflex responses induced by alpha(2)-adrenergic agents is due to action on al pha-motoneurons or peripheral nociceptors, we studied the effect of me detomidine, an alpha(2)-adrenoceptor agonist, on the monosynaptic refl ex and on the primary afferent nociceptor-mediated antidromic vasodila tor response in rats. Additionally, the effect on the dorsal root pote ntial, an index of a transient excitability change in the central term inals of primary afferent fibers, was determined. Medetomidine was app lied systemically at doses (100 and 300 mu g/kg) which have proven str ongly antinociceptive in previous studies. The amplitudes of a submaxi mal monosynaptic reflex volley or a submaximal dorsal root potential w ere not changed by medetomidine. Medetomidine induced a decrease of cu taneous blood flow but did not abolish the vasodilatatory response to antidromic stimulation of the sciatic nerve at C-fiber intensity as de termined by the laser Doppler flow method. The results indicate that t he alpha(2)-adrenoceptor-mediated suppression of nocifensive reflex re sponses is not caused by a decreased excitability of motoneurons or pe ripheral nociceptors. An alpha(2)-adrenoceptor agonist does not modula te the transient stimulus-evoked change in the excitability of central terminals of primary afferent fibers.