Prepulse modulation of the startle reaction and the blink reflex in normal human subjects

Blink reflexes are usually considered the most representative and consistent response of the auditory startle reaction (ASR), and they are often the only response evaluated in human psychophysiological studies. However, auditory stimuli also induce an auditory blink reflex (ABR), the physiological characteristics and brainstem circuitry of which may be different from those of the ASR. This study aimed to investigate whether there were differences between the orbicularis oculi (OOc) responses elicited with the ABR (OOcABR) and those elicited with the ASR (OOcASR) regarding their behavior to prepulse modulation. For comparison, we also examined the OOc responses to supraorbital nerve stimulation (OOcEBR). Electromyographic responses were simultaneously recorded from the OOc, masseter (MAS) and sternocleidomastoid (SCM) muscles. ABRs were considered when auditory stimuli induced responses limited to the OOc, and ASRs were considered when responses were induced in all muscles recorded from. Prepulse stimuli were either a weak electrical stimulation at the third finger (somatosensory prepulse) or a weak acoustic tone (auditory prepulse) that preceded the response-eliciting stimuli by intervals ranging from 0 to 200 ms. Prepulse effects differed according to prepulse modality, but the OOcABR and the OOcASR were always modulated in the same way. In both responses, somatosensory prepulses induced facilitation from 20 to 50 ms, followed by inhibition beyond 75 ms, and auditory prepulses induced no facilitation but a significant inhibition beyond 30 ms. In the OOcEBR, both somatosensory and acoustic prepulses induced facilitation of R1 and inhibition of R2 beyond 30 ms. Our results suggest that the OOcABR and the OOcASR exhibit the same physiological behavior regarding prepulse modulation. It is hypothesized that prepulse facilitation is due to direct impingement of subthreshold excitatory inputs onto the facial motoneurons while prepulse inhibition results from the engagement of a presynaptic inhibitory circuit in the brainstem.