Antinociceptive Activity ofTrichilia catiguaHydroalcoholic Extract: New Evidence on Its Dopaminergic Effects
Alice Fialho VianaIzaque de Sousa MacielEmerson Marcelo MottaPaulo César LealLuiz F. PianowskiMaria M. CamposJoão Β. Calixto
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Abstract:
Trichilia catigua is a native plant of Brazil; its barks are used by some local pharmaceutical companies to prepare tonic drinks, such as Catuama. The present study was addressed to evaluate the effects of T. catigua hydroalcoholic extract in mouse nociception behavioral models, and to evaluate the possible mechanisms involved in its actions. Male Swiss mice were submitted to hot-plate, writhing and von Frey tests, after oral treatment with T. catigua extract (200 mg kg(-1), p.o.). The extract displayed antinociceptive effect in all three models. For characterization of the mechanisms involved in the antinociceptive action of the extract, the following pharmacological treatments were done: naloxone (2.5 mg kg(-1), s.c.), SR141716A (10 mg kg(-1), i.p.), SCH23390 (15 μg kg(-1), i.p.), sulpiride (50 mg kg(-1), i.p.), prazosin (1 mg kg(-1), i.p.), bicuculline (1 mg kg(-1), i.p.) or dl-p-chlorophenylalanine methyl ester (PCPA, 100 mg kg(-1), i.p.). In these experiments, the action of T. catigua extract was evaluated in the hot-plate test. The treatment with SCH23390 completely prevented the antinociceptive effect, while naloxone partially prevented it. The possible involvement of the dopaminergic system in the actions of T. catigua extract was substantiated by data showing the potentiation of apomorphine-induced hypothermia and by the prevention of haloperidol-induced catalepsy. In conclusion, the antinociceptive effects of T. catigua extract seem to be mainly associated with the activation of dopaminergic system and, to a lesser extent, through interaction with opioid pathway.Keywords:
Catalepsy
Apomorphine
Sulpiride
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Caudate nucleus
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Drug effects on behaviour are closely related to the temporal patterns of their administration. Numerous studies have demonstrated that regular (daily) versus intermittent dosing of any drug can determine whether tolerance or sensitization is developed. The aim of this study was to examine if daily (10 days) or intermittent (every other day and every two days) administration of haloperidol (0.75 mg/kg, ip) could affect differentially to catalepsy of male (experiment 1) and female mice (experiment 2). Catalepsy was measured by means of the 'bar test', being evaluated 120 minutes after the last administration of haloperidol or saline. In both experiments, as compared with controls, catalepsy increased significantly in mice treated with a single injection of haloperidol, as well as in the groups treated with haloperidol intermittently, although a marked tolerance to haloperidol-induced catalepsy after daily administration of the drug was observed. However, only the group of female mice treated with haloperidol every two days showed significantly more catalepsy than those treated daily or every other day, suggesting that the effect of several schedules of drug administration can affect differentially to male and female mice.
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Summary In a double-blind cross-over trial, 20 chronic schizophrenic patients were treated with sulpiride and haloperidol in two 12-week periods. The final median dose of sulpiride was 2000 mg/day (range 800–3200) and of haloperidol 12 mg/day (range 6–24). Sulpiride had an antipsychotic effect and therapeutic profile not significantly different from that of haloperidol. In spite of the high doses of sulpiride, extrapyramidal side-effects were seen less frequently during the first four weeks of the sulpiride period than during the corresponding haloperidol period ( P < 0.05), whereas autonomic side-effects were equally rare for both drugs. A positive correlation was found between daily dose and plasma concentration of both sulpiride ( P < 0.001) and haloperidol ( P < 0.05), but no correlation could be established between clinical effects and plasma levels of either neuroleptic.
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To investigate the memory-enhancing drugs piracetam, vinpocetine, and ginkgo biloba for their ability to reduce catalepsy in mice treated with haloperidol. Haloperidol is a classic neuroleptic drug that induces motor abnormalities and cognitive impairment due to a blockade of dopamine D2 receptors in the striatum. Materials and methods: Catalepsy was induced by intraperitoneal haloperidol (2 mg/kg) administration. The drugs being tested were either administered intraperitoneally (IP) along with the dosage of haloperidol or 30 min prior to the introduction of the haloperidol. Catalepsy was measured using the bar test. Results: The administration of haloperidol (2 mg/kg, IP) resulted in significant catalepsy. Piracetam (in dosages of 50, 100, and 300 mg/kg) given IP at the time of haloperidol administration reduced the duration of catalepsy by 24.4%, 32.3%, and 48.2%, respectively. Piracetam given as a 30-min pretreatment reduced the duration of catalepsy by 59.5%, 72.3%, and 78.2%, respectively. Vinpocetine coadministered IP with haloperidol did not modify catalepsy, but given as a 30-min pretreatment, the drug increased catalepsy duration by 53.5%, 53.6%, and 65.1%, respectively. Ginkgo biloba coadministered IP with haloperidol at 25, 50, or 150 mg/kg increased catalepsy duration by 13.6%-17.1%. Ginkgo biloba given 30 min prior to haloperidol increased catalepsy duration by 29.1%, 35.1%, and 37.2%, respectively. Conclusion: The present study indicates that the nootropic drug piracetam reduces haloperidol-induced catalepsy in mice.
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Sixteen young (5 months) and 16 old (20-24 months) male Wistar rats, housed together or in individual cages were observed for cataleptic behavior 10, 20 and 30 days after the beginning of chronic haloperidol treatment (1.0 mg/kg, twice daily, for 30 days). Catalepsy was measured by the bar test. Age increased the duration of haloperidol-induced catalepsy of isolated and group-housed rats in the three observation sessions (old-isolated = 7.4 +/- 0.2; old-group housed = 7.5 +/- 0.1; young-isolated = 6.3 +/- 0.2; young-group housed = 6.8 +/- 0.2 In seconds in session 1, for example). Conversely, isolation did not modify the sensitivity to the cataleptic effect of haloperidol. Even more important, no differences in duration of haloperidol-induced catalepsy were observed among the three sessions for each group. The results indicate that under the experimental conditions employed the animals did not develop tolerance nor sensitization to haloperidol-induced catalepsy. In addition, neither age nor isolation modified the absence of effects of repeated haloperidol treatment on the catalepsy behavior of rats.
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