THE TRIGEMINALLY EVOKED BLINK REFLEX .2. MECHANISMS OF PAIRED-STIMULUS SUPPRESSION

The paired-stimulus paradigm, presentation of a pair of identical refl ex-eliciting stimuli to the supraorbital nerve (SO) with an interstimu lus interval of less than 2 s, evokes a response to the second, test, stimulus which is less than that elicited by the first, conditioning, stimulus. In this study, we investigated the site of this suppression and its pharmacology in the alert guinea pig. Both the early (R1) and the late (R2) component of the SO-evoked blink reflex exhibited suppre ssion in the paired-stimulus paradigm. Initiation of suppression appea red to be specific to the afferent limb of the reflex rather than the result of motor activity generated by the conditioning stimulus. Neith er acoustic conditioning stimuli nor air puffs that elicited blinks vi a another branch of the trigeminal nerve suppressed the test response. Extremely weak SO shocks, however, that did not directly elicit a ref lex, caused suppression of the response to subsequent SO stimuli of no rmal intensity. Paired stimulus suppression of the R1 component appear ed to involve activation of GABA(A) receptors within the spinal trigem inal nucleus. Both systemic injections and microinjections of baclofen into the spinal trigeminal nucleus enhanced R1 suppression, whereas i dentical injections of CGP35348, a GABA(B) antagonist, diminished R1 s uppression. Furthermore, single-unit recordings in alert animals revea led that spinal trigeminal neurons exhibited suppression in the paired -stimulus paradigm that resembled that of the R1 component of the blin k reflex. These findings showed that sensory gating underlies paired-s timulus suppression of the SO-evoked blink reflex and that activation of GABA(A) receptors plays an important role in this process.