Reflexes are useful tools with which to study the mechanisms the nervous system uses to control its responsiveness. This dissertation characterizes the neural circuitry which generates the blink reflex and the mechanisms by which the reflex is suppressed by presentation of a prior stimulus. The results indicate that this suppression occurs at the afferent limb of the reflex arc and involves activation of GABAb receptors.; Blinks were evoked in guinea pigs by stimulating the supraorbital branch of the trigeminal nerve (S.O.) and recording the electromyograph (EMG) in the orbicularis oculi (OO). Blinks consisted of two bursts of EMG activity: R1, with a latency of about 7 ms, and R2, with a latency of about 17 ms. Activation of A{dollar}beta{dollar} afferents appeared sufficient to elicit R1 and R2, but activation of A{dollar}delta{dollar} fibers might enhance both responses.; Anatomical experiments, lesions and localized injections of pharmacological agents delineated separate neural circuits for R1 and R2. The S.O. nerve projected densely to the C1 dorsal horn and moderately to the spinal trigeminal nucleus (SpV). Hemisections at C1 eliminated R2 but not R1; subsequent hemisections at SpV eliminated R1. Microinjections of the GABAb agonist baclofen into SpV eliminated R1 but not R2. Thus, SpV participates in R1, whereas C1 participates in R2.; Presentation of a reflex-eliciting conditioning S.O. stimulus 2 or less seconds before an identical test stimulus suppressed R1 and R2 test responses. I investigated the source, pharmacology and site of this suppression. Initiation of suppression appeared to be afferent specific and not due to motor activity generated by the conditioning stimulus. Neither acoustic conditioning stimuli nor air puffs which elicited blinks via another branch of the trigeminal nerve, suppressed the test S.O. blink. However, extremely weak S.O. shocks, which did not directly elicit a reflex, did initiate some suppression. R1 suppression appeared to involve activation of GABAb receptors within SpV. Both systemic injections and SpV microinjections of baclofen enhanced R1 suppression, whereas such injections of CGP 35348, a GABAb antagonist, diminished R1 suppression. Furthermore, SpV neurons exhibited suppression which resembled that of R1.
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