Navegando por Palavras-chave "colículo inferior"

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    Participação do substrato neural glutamatérgico do colículo inferior sobre a catalepsia induzida pela microinjeção intraestriatal de haloperidol
    (Universidade Federal de São Paulo (UNIFESP), 2013-02-27) Medeiros, Priscila de [UNIFESP]; Melo, Liana Lins Melo [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    The inferior colliculus (IC), a midbrain structure that processes acoustic information of aversive nature, is distinguished from other auditory nuclei in the brainstem by its connections with structures of the motor system. The glutamate is the main excitatory neurotransmitters of central nervous system (CNS) and any studies has showed the participate of neurotransmission in the IC. Studies have shown that microinjection of Nmethyl-D-aspartate (NMDA), a glutamate agonist, in the central nucleus of the IC of rats promotes defensive reactions such as running, jumping and surveys, interspersed by a state of intense stillness. The present study investigated the influence of excitatory amino acid-mediated mechanisms in the inferior colliculus on the catalepsy induced by intrastriatal microinjection of haloperidol (10μg/0.5µl) in rats. Male wistar rats were bilaterally implanted with stainless steel guide cannula in the IC and dorsomedial striatum or ventralmedial. After recovery from surgery, the animals received bilateral intracollicular microinjections of the NMDA receptor agonist N-methyl-D-aspartate (NMDA 10 or 20nmol/0.5 µl) or of physiological saline (0.5 µl) into the dorsalmedial striatum or the NMDA receptor antagonists MK-801 (15 or 30mmol /0.5 µl) or of physiological saline (0.5 µl). After 5 minutes all animals received intraestriatal bilateral microinjections of haloperidol (10 µg/ 0.5 µl) or vehicle (0.5 µl). The rats were tested for catalepsy by carefully positioning their forepaws on a horizontal wooden bar 8 cm height above the floor and the latency for stepping down was measured at 0, 30, 60, 90 and 120 min after haloperidol administration. Results showed that administration of physiological saline into the ICs followed by microinjection of haloperidol in the dorsomedial region of the striatum was not able to induce catalepsy. However, when the administration of NMDA in bilateral CIs was followed by microinjection of haloperidol dorsomedial striatum was observed a significant catalepsy. The antagonist MK-801 when administered into the ICs, was able to reduce the time of catalepsy in the animals receiving haloperidol in the ventromedial striatum. Our results point to a possible involvement of the IC in the intraestriatal haloperidol-induced catalepsy, suggesting the involvement of a glutamatergic neural substrate in this circuit. It is possible that the IC influences the state of immobility produced by weakening the nigrostriatal dopaminergic neurotransmission.