Lesions of the rat entopeduncular nucleus further deteriorate N-methyl-D-aspartate receptor antagonist-induced deficient prepulse inhibition.

Abstract

Lesions of the rat entopeduncular nucleus (EPN), the equivalent to the human globus pallidus internus (GPi), have been shown to improve deficient prepulse inhibition (PPI) induced by the dopamine agonist apomorphine. We here tested the effect of EPN lesions on the PPI-disruptive effect of the non-competitive NMDA receptor antagonist dizocilpine in rats. Neurotoxic bilateral lesions of the EPN were induced by ibotenic acid (4 μg in 0.4 μl). Rats were tested for PPI and locomotor activity after systemic injection of dizocilpine (vehicle and 0.15 mg/kg). Bilateral EPN lesions further deteriorated the PPI deficit induced by dizocilpine, while locomotion was not affected. This work indicates that the EPN is an important brain region within the neuronal circuit responsible for NMDA receptor antagonist-induced PPI deficits.