The acoustic startle reflex is a coordinated contraction of the skeletal musculature in response to a sudden, intense sound. One form of startle 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 an operational measure of sensorimotor gating, and is significantly impaired in several neuropsychiatric disorders that are characterized by symptoms associated with central inhibitory deficits. In rats, prepulse inhibition is disrupted by central dopamine activation or by manipulations of limbic cortical structures including the prefrontal cortex and hippocampus. In the present study, we assessed prepulse inhibition in rats after surgical and pharmacologic manipulations of the basolateral amygdala. Quinolinic acid lesions of the basolateral amygdala significantly reduced prepulse inhibition without significantly changing startle amplitude. These lesions also blocked fear-potentiated startle, which is known to be regulated by the basolateral amygdala. The prepulse inhibition-disruptive effects of basolateral amygdala lesions were not reversed by systemic injection of the dopamine antagonist haloperidol at doses that totally restored prepulse inhibition in apomorphine-treated rats. In other studies, intra-amygdala infusion of the competitive N-methyl-D-aspartate antagonist DL-2-amino-5-phosphonovaleric acid (0, 0.15, 1.5, 4.5 microg) dose-dependently reduced prepulse inhibition. These data suggest that the basolateral amygdala regulates sensorimotor gating by mechanisms that are independent of central dopamine hyperactivity.