Navegando por Palavras-chave "catalepsy"

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    Behavioral effects of MK-801 on reserpine-treated mice
    (Elsevier B.V., 2002-04-01) Dutra, R. C.; Andreazza, A. P.; Andreatini, R.; Tufik, Sergio [UNIFESP]; Vital, Maria ABF [UNIFESP]; Univ Fed Parana; Universidade Federal de São Paulo (UNIFESP)
    The effects of dizocilpine (MK-801), a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, were studied on dopamine-related behaviors induced by reserpine treatments. This study focuses on behavioral syndromes that may used as models for Parkinson's disease, or tardive dyskinesia, and its response after glutamatergic blockage. Reserpine (1 mg/kg), administered once every other day for 4 days, produced increases in orofacial dyskinesia, tongue protrusion and vacuous chewing in mice, which are signs indicative of tardive dyskinesia. Reserpine also produced tremor and catalepsy, which are signs suggestive of Parkinson's disease. MK-801 (0.1 mg/kg), administered 30 min before the observation test, prevented the vacuous chewing movements., tongue protrusions and catalepsy induced by reserpine. However, MK-801 injection produced a significant increase of tremor in reserpine-treated mice. Reserpine (1 mg/kg), administered 90 min before the test and followed by apomophine injection (0.1 mg/kg) 5 min before the test, did not produce oral dyskinesia in mice. On the other hand, reserpine induced increases in tremor and catalepsy compared to control mice. MK-801 (0.1 mg/kg) administration attenuated the catalepsy and tremor induced by reserpine. Pretreatment with reserpine (1 mg/kg) 24 h before the observation test produced increases in vacuous chewing movements and tongue protrusion, as well as increases in tremor and catalepsy, whereas MK-801 (0.1 mg/kg) injection 90 min before the test reversed the effects of reserpine, These results show that reserpine produces different and abnormal movements, which are related to dose and schedule employed and can be considered as parkinsonian-like and tardive dsykinesia signs. the glutamatergic blockage produced by NMDA can restore these signs, such as vacuous chewing movements, tongue protrusions, catalepsy and tremor according to the employed model. (C) 2001 Elsevier Science Inc. All rights reserved.
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    MODULATION 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 INEC
    Not 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.
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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.