Glutamatergic neurotransmission in the inferior colliculus influences intrastriatal haloperidol-induced catalepsy

• Published in: Behavioural brain research Vol. 268; pp. 8 - 13
• Main Authors: Medeiros, P., Viana, M.B., Barbosa-Silva, R.C., Tonelli, L.C., Melo-Thomas, L.
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier B.V 15-07-2014; Elsevier
• Subjects: Animals; Antipsychotic Agents - adverse effects; Biological and medical sciences; Catalepsy; Catalepsy - chemically induced; Catalepsy - physiopathology; Corpus Striatum - drug effects; Corpus Striatum - physiopathology; Dizocilpine Maleate - pharmacology; Ear and associated structures. Auditory pathways and centers. Hearing. Vocal organ. Phonation. Sound production. Echolocation; Excitatory Amino Acid Antagonists - pharmacology; Fundamental and applied biological sciences. Psychology; Glutamate; Glutamic Acid - metabolism; Haloperidol; Haloperidol - adverse effects; Inferior colliclus; Inferior Colliculi - drug effects; Inferior Colliculi - physiopathology; Male; Medical sciences; N-Methylaspartate - metabolism; Neuropharmacology; NMDA; Pharmacology. Drug treatments; Psycholeptics: tranquillizer, neuroleptic; Psychology. Psychoanalysis. Psychiatry; Psychopharmacology; Rats, Wistar; Receptors, N-Methyl-D-Aspartate - agonists; Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors; Receptors, N-Methyl-D-Aspartate - metabolism; Striatum; Synaptic Transmission - drug effects; Synaptic Transmission - physiology; Vertebrates: nervous system and sense organs; NMDA; Striatum; Inferior colliclus; Haloperidol; Glutamate; Catalepsy; Psychotropic; Neuroleptic; Central nervous system; Basal ganglion; Corpus striatum; Encephalon; Colliculus inferior; Excitatory aminoacid; Neurotransmitter; Auditory pathway; Neurotransmission
• DOI: 10.1016/j.bbr.2014.03.027
• EISSN: 1872-7549
• ISSN: 0166-4328

•A modulation of the IC in the catalepsy induced by haloperidol is proposed.•The IC plays a role in sensorimotor gating and glutamatergic mechanisms are involved.•MK-801 injected in the IC reduced ventral striatum haloperidol-induced catalepsy.•NMDA injected in the IC facilitated dorsal striatum haloperidol-induced catalepsy.•The IC integrates information from the auditory system and influences motor output.
The inferior colliculus (IC) is an important midbrain relay station for the integration of descending and ascending auditory information. In addition, it has also been implicated in the processing of acoustic information of aversive nature, as well as in sensory-motor gating. There is evidence that glutamate-mediated mechanisms at the IC level influence haloperidol-induced catalepsy. The present study investigated the influence of glutamate-mediated mechanisms in the IC on catalepsy induced by intrastriatal microinjection of haloperidol (10μg/0.5μl). Male Wistar rats received bilateral intracollicular microinjections of the glutamate receptor agonist NMDA (10 or 20nmol/0.5μl), the NMDA receptor antagonists MK-801 (15 or 30nmol/0.5μl) or physiological saline (0.5μl), followed by bilateral microinjections of haloperidol (10μg/0.5μl) or vehicle (0.5μl) into the dorso-rostral or ventro-rostral striatum. The catalepsy test was performed positioning both forepaws of the rats on an elevated horizontal wooden bar and recording the time during which the animal remained in this position. The results showed that the administration of physiological saline in the IC followed by the microinjection of haloperidol in the dorso-rostral region of the striatum was not able to induce catalepsy. However, when the bilateral administration of NMDA into the IC was followed by microinjection of haloperidol into the dorso-rostral striatum, catalepsy was observed. The microinjection of haloperidol into the ventro-rostral striatum induced catalepsy, counteracted by previous administration of MK-801 into the IC. These findings suggest that glutamate-mediated mechanisms in the IC can influence the intrastriatal haloperidol-induced catalepsy and that the IC plays an important role as a sensorimotor interface.