THE BASOLATERAL AMYGDALA REGULATES SENSORIMOTOR GATING OF ACOUSTIC STARTLE IN THE RAT

The acoustic startle reflex is a coordinated contraction of the skelet al musculature in response to a sudden, intense sound. One form of sta rtle plasticity, ''prepulse inhibition'', is the normal suppression of the startle reflex when the intense startling stimulus is immediately preceded by a weak pre-stimulus. Prepulse inhibition is utilized as a n operational measure of sensorimotor gating, and is significantly imp aired in several neuropsychiatric disorders that are characterized by symptoms associated with central inhibitory deficits. In rats, prepuls e inhibition is disrupted by central dopamine activation or by manipul ations of limbic cortical structures including the prefrontal cortex a nd hippocampus. In the present study, we assessed prepulse inhibition in rats after surgical and pharmacologic manipulations of the basolate ral amygdala. Quinolinic acid lesions of the basolateral amygdala sign ificantly reduced prepulse inhibition without significantly changing s tartle amplitude. These lesions also blocked fear-potentiated startle, which is known to be regulated by the basolateral amygdala. The prepu lse inhibition-disruptive effects of basolateral amygdala lesions were not reversed by systemic injection of the dopamine antagonist haloper idol at doses that totally restored prepulse inhibition in apomorphine -treated rats. In other studies, intra-amygdala infusion of the compet itive N-methyl-D-aspartate antagonist DL-2-amino-5-phosphonovaleric ac id (0, 0.15, 1.5, 4.5 mu g) dose-dependently reduced prepulse inhibiti on. These data suggest that the basolateral amygdala regulates sensori motor gating by mechanisms that are independent of central dopamine hy peractivity. Copyright (C) 1996 IBRO.