Navegando por Palavras-chave "inferior colliculus"
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- ItemSomente MetadadadosCB1 cannabinoid receptor-mediated anandamide signaling mechanisms of the inferior colliculus modulate the haloperidol-induced catalepsy(Pergamon-Elsevier Science Ltd, 2016) Medeiros, Priscila [UNIFESP]; de Freitas, R. L.; Silva, M. O.; Coimbra, N. C.; Melo-Thomas, Liana [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. Previous evidence relating the IC to motor behavior shows that glutamatergic and GABAergic mechanisms in the IC exert influence on systemic haloperidol-induced catalepsy. There is substantial evidence supporting a role played by the endocannabinoid system as a modulator of the glutamatergic neurotransmission, as well as the dopaminergic activity in the basal nuclei and therefore it may be considered as a potential pharmacological target for the treatment of movement disorders. The present study evaluated if the endocannabinoid system in the IC plays a role in the elaboration of systemic haloperidol-induced catalepsy. Male Wistar rats received intracollicular microinjection of either the endogenous cannabinoid anandamide (AEA) at different concentrations (5, 50 or 100 pmol/0.2 mu l), the CB1 cannabinoid receptor antagonist AM251 at 50, 100 or 200 pmol/0.2 mu l or vehicle, followed by intraperitoneal (IP) administration of either haloperidol at 0.5 or 1 mg/kg or physiological saline. Systemic injection of haloperidol at both doses (0.5 or 1 mg/kg, IP) produced a cataleptic state, compared to vehicle/physiological saline-treated group, lasting 30 and 50 min after systemic administration of the dopaminergic receptors non-selective antagonist. The midbrain microinjection of AEA at 50 pmol/0.2 mu l increased the latency for stepping down from the horizontal bar after systemic administration of haloperidol. Moreover, the intracollicular administration of AEA at 50 pmol/0.2 mu l was able to increase the duration of catalepsy as compared to AEA at 100 pmol/0.2-mu l-treated group. Intracollicular pretreatment with AM251 at the intermediate concentration (100 pmol/0.2 mu l) was able to decrease the duration of catalepsy after systemic administration of haloperidol. However, neither the intracollicular microinjection of AM251 at the lowest (50 pmol/0.2 mu l) nor at the highest (200 pmol/0.2 mu l) concentration was able to block the systemic haloperidol-induced catalepsy. Furthermore, the intracollicular administration of AM251 at 100 pmol/0.2 mu l was able to decrease the duration of catalepsy as compared to AM251 at 50 pmol/0.2 mu l- and AM251 at 200 pmol/0.2-mu l-treated group. The latency for stepping down from the horizontal bar-induced by haloperidol administration-was decreased when microinjection of AEA at 50 pmol/0.2 mu l was preceded with blockade of CB1 receptor with AM251 (100 pmol/0.2 mu l). Our results strengthen the involvement of CB1-signaled endocannabinoid mechanisms of the IC in the neuromodulation of catalepsy induced by systemic administration of the dopaminergic receptors non-selective antagonist haloperidol. (C) 2016 IBRO. Published by Elsevier Ltd. All rights reserved.
- ItemSomente MetadadadosMODULATION of HALOPERIDOL-INDUCED CATALEPSY in RATS BY GABAERGIC NEURAL SUBSTRATE in the INFERIOR COLLICULUS(Elsevier B.V., 2013-12-26) Tostes, J. G.; Medeiros, P. [UNIFESP]; Melo-Thomas, L. [UNIFESP]; Univ Sao Francisco; Fac Med Itajuba; Universidade Federal de São Paulo (UNIFESP); Inst Neurociencias & Comportamento INECNot only is the inferior colliculus (IC) a highly important center of integration within the central auditory pathway, but it may also play a modulatory role in sensorymotor circuitry. Previous evidence from our laboratory relating the IC to motor behavior shows that glutamate-mediated mechanisms within the IC modulate haloperidol-induced catalepsy. the high density of GABAergic receptors in the IC led to this study of a possible link between these receptors, haloperidol-induced catalepsy, and a possible involvement of the blockade of dopaminergic receptors. Catalepsy was evaluated by positioning both forepaws of rats on an elevated horizontal wooden bar and recording the time that the animal maintained this position. the present study shows that haloperidol-induced catalepsy was enhanced by local microinjection into the IC of midazolam (20 nmol/0.5 mu l), a benzodiazepine receptor agonist, whereas animals receiving a microinjection of bicuculline (40 or 80 ng/0.5 mu l), a GABAergic antagonist, showed a reduction in the time of catalepsy. However, the microinjection of haloperidol (2.5 or 5.0 mu g/0.5 mu l) bilaterally into the IC did not induce catalepsy. Therefore, our results suggest the involvement of the IC in the modulation of catalepsy induced by haloperidol, even though the dopaminergic mechanisms of the IC are unable to induce catalepsy when blocked by the direct microinjection of haloperidol. It is thus possible that the IC plays a role in sensorimotor gating and that GABA-mediated mechanisms are involved. (C) 2013 IBRO. Published by Elsevier B.V. All rights reserved.
- ItemSomente MetadadadosParticipação 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.