Glutamatergic neurotransmission mediated by NMDA receptors in the inferior colliculus can modulate haloperidol-induced catalepsy.

The inferior colliculus (IC) is primarily involved in the processing of auditory information, but it is distinguished from other auditory nuclei in the brainstem by its connections with structures of the motor system. Functional evidence relating the IC to motor behavior derives from experiments showing that activation of the IC by electrical stimulation or excitatory amino acid microinjection causes freezing, escape-like behavior, and immobility. However, the nature of this immobility is still unclear. The present study examined the influence of excitatory amino acid-mediated mechanisms in the IC on the catalepsy induced by the dopamine receptor blocker haloperidol administered systemically (1 or 0.5 mg/kg) in rats. Haloperidol-induced catalepsy was challenged with prior intracollicular microinjections of glutamate NMDA receptor antagonists, MK-801 (15 or 30 mmol/0.5 microl) and AP7 (10 or 20 nmol/0.5 microl), or of the NMDA receptor agonist N-methyl-d-aspartate (NMDA, 20 or 30 nmol/0.5 microl). The results showed that intracollicular microinjection of MK-801 and AP7 previous to systemic injections of haloperidol significantly attenuated the catalepsy, as indicated by a reduced latency to step down from a horizontal bar. Accordingly, intracollicular microinjection of NMDA increased the latency to step down the bar. These findings suggest that glutamate-mediated mechanisms in the neural circuits at the IC level influence haloperidol-induced catalepsy and participate in the regulation of motor activity.

Effects of lesions of amygdaloid nuclei and substantia nigra on aversive responses induced by electrical stimulation of the inferior colliculus.

Stimulation of the central nucleus of the inferior colliculus causes defensive behavior. In this work we examined the influence of lesions of brain structures involved in the expression of fear, such as periaqueductal gray matter, amygdala, and substantia nigra pars reticulata (SNpr), on these aversive responses. Thus, rats were implanted with an electrode in the central nucleus of the inferior colliculus, for the determination of the thresholds of alertness, freezing, and escape responses. Each rat also bore a cannula implanted in the periaqueductal, amygdala or Snpr for injection of the neurotoxin N-methyl-D-aspartate (8 micrograms/0.8 microliters). The data obtained show that lesion of the central nucleus of the amygdala increases the thresholds of aversive responses whereas lesion of the basolateral complex decreases the threshold of these responses. Lesion of the Snpr increased the aversive consequences of the electrical stimulation of the inferior colliculus whereas periaqueductal gray lesions, either dorsal or ventral regions, did not change these responses. From the evidences obtained in this work, it is suggested that the expression of the defensive behavior induced by activation of the neural substrates of the inferior colliculus does not seem to depend on the integrity of the periaqueductal gray. On the contrary, the basolateral complex inhibits and the central nucleus amplifies the aversive responses integrated in the inferior colliculus. Furthermore, SNpr seems also to be an important motor output for the defensive behavior induced by stimulation of the inferior colliculus, in agreement with what has been suggested for other brain structures implicated in the expression of fear.