ALPHA(2)-ADRENOCEPTORS MODULATE NMDA-EVOKED RESPONSES OF NEURONS IN SUPERFICIAL AND DEEPER DORSAL HORN OF THE MEDULLA

Extracellular single unit recordings were made from neurons in the sup erficial and deeper dorsal horn of the medulla (trigeminal nucleus cau dalis) in 21 male rats anesthetized with urethan. NMDA produced an ant agonist-reversible excitation of 46 nociceptive as well as nonnocicept ive neurons. Microiontophoretic application of a preferential alpha(2) -adrenoceptor (alpha(2)AR) agonist, (2-[2,6-dichloroaniline]-2-imidazo line) hydrochloride (clonidine), reduced the NMDA.-evoked responses of 86% (6/7) of nociceptive-specific (NS) neurons, 82% (9/11) of wide dy namic range (WDR) neurons, and 67% (4/6) of low-threshold (LT) neurons in the superficial dorsal horn. In the deeper dorsal horn, clonidine inhibited the NMDA-evoked responses of 94% (16/17) of NS and WDR neuro ns and 60% (3/5) of LT neurons. Clonidine facilitated the NMDA-evoked responses in 14% (1/17) of NS, 9% (1/11) of WDR. and 33% (2/6) of LT n eurons in the superficial dorsal horn. Idazoxan, an alpha(2)AR antagon ist, reversed the inhibitory effect of clonidine in 90% (9/10) of neur ons, whereas prazosin, an alpha(1)-adrenoceptor antagonist with affini ty for alpha(2B)AR, and alpha(2C)AR, were ineffective. We suggest that activation of alpha(2)ARs produces a pre dominantly inhibitory modula tion of the NMDA-evoked responses of nociceptive neurons in the medull ary dorsal horn.