Involvement of the glutamatergic neurotransmission in the inferior colliculus on the catalepsy induced by intraestriatal haloperidol microinjection

Abstract

The inferior colliculus (IC) is primarily involved in auditory information processing but also integrates sensory information of aversive nature. Aberrant processing of auditory information may be at the root of auditory delusions commonly seen in schizophrenic patients. It has been shown that that the activation of the neural substrates of aversion of the IC by excitatory amino acids (EAA) causes freezing, escape behavior and tonic immobility and that the electrical stimulation of the IC increases the extracellular levels of dopamine in the frontal cortex. However, the nature of this tonic immobility and how it relates with catalepsy induced by dopamine receptor blockers such as the haloperidol are unclear. This study will examine the influence of EAA-mediated mechanisms of the IC on the catalepsy induced by intrastriatal microinjection of haloperidol (2.5¼g/0.5µl). To this end, haloperidol-induced catalepsy will be challenged with prior intracollicular microinjections of MK-801(2.5 or 5µg/0.5µl), AP7 (10 or 20 nmol/0.5µl) or NMDA (20 or 30 nmol/0.5µl). Immediately after the time of catalepsy will be measured.