THE TRIGEMINALLY EVOKED BLINK REFLEX .1. NEURONAL CIRCUITS

In this study, we characterized the pathways that generate the trigemi nal blink reflex in the guinea pig. Blinks were evoked by stimulation of the supraorbital branch of the trigeminal nerve and measured by rec ording electromyographic activity in the lid-closing orbicularis oculi muscle (OOemg) and, in one case, lid position. Blinks evoked by stimu lation of the supraorbital nerve consisted of two bursts of muscle act ivity ipsilateral to the side of stimulation. The first, R1, had a lat ency of 6.9 ms and the second, R2, had a latency of 17.25 ms. Increasi ng stimulus intensity to 3 times threshold for evoking an ipsilateral blink elicited an R1 and R2 response contralaterally, with latencies o f 9.2 ms and 19.25 ms, respectively. We investigated the causes for th is bipartite response that is seen in the guinea pig, as well as other mammals including humans. The two-component response could arise from different populations of afferents, or from different central circuit s, or a combination of these two causes. Multiunit recording in the tr igeminal ganglion and simultaneous measurement of the OOemg showed tha t activation of AP afferents alone was sufficient to elicit both the R 1 and the R2 responses, but that activation of A delta afferents could enhance both responses. Different neural circuits, however, produce t he R1 and R2 responses. Transganglionic tracing with wheatgerm aggluti n or choleragenoid subunit of cholera toxin bound to HRP revealed that primary afferents from the supraorbital branch of the trigeminal nerv e terminated densely in the dorsal horn of spinal cord segment C1 and in the caudalis-interpolaris border region of the spinal trigeminal nu cleus. Injections of HRP into the orbicularis oculi motoneuron region of the facial nucleus showed that both of these regions projected to t he facial nucleus. Hemisections at the level of C1 eliminated the R2 b link response, but not the R1 response, evoked by stimulation of the s upraorbital branch of the trigeminal nerve. Subsequent hemisections at the level of the obex eliminated the R1 response. Microinjections of the GABA(B) agonist baclofen into the spinal trigeminal nucleus at the level of the obex abolished the R1 but not the R2 response. Thus, the spinal trigeminal nucleus produces the R1 component, whereas the R2 c omponent originates in the C1 region of the spinal cord.