apomorphine/hypersensitivity

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Effect of daily dose of chronic haloperidol and chronic apomorphine on behavioral hypersensitivity in the rat.

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Behavioral hypersensitivity in the rat consisting of increased dopamine-mediated stereotypic behaviors has been found to follow a 10-day course of treatment with the neuroleptic haloperidol as well as with the direct dopamine agonist apomorphine. The daily dose versus response relationship for

Differential liabilities of haloperidol and thioridazine for inducing apomorphine hypersensitivity.

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In an animal model of tardive dyskinesia, sensitivity to apomorphine-induced stereotyped behavior reflects increased dopamine receptor activity induced by chronic neuroleptic treatment. Four groups of Sprague-Dawley rats received haloperidol (H) 0.5 mg/kg, haloperidol 0.5 mg/kg + benztropine 2.0

Hypophysectomy-induced striatal hypersensitivity and mesolimbic hyposensitivity to apomorphine.

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Seven days post-hypophysectomy female rats display a hyposensitivity to the locomotor effects of apomorphine and a hypersensitivity to the stereotypy effects of apomorphine, while at 28 days post-hypophysectomy they are hypersensitive to both the locomotor and stereotypy effects of apomorphine. The

[Hypersensitivity to apomorphine in rats treated with neuroleptics: a model of tardive dyskinesia].

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Chronic benztropine and haloperidol administration induce behaviorally equivalent pharmacological hypersensitivities separately but not in combination.

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This study reports the pharmacologic induction of behavioral pharmacologic hypersensitivity in an animal model of tardive dyskinesia. Four groups of rats received IP injections twice daily of 2.5 mg/kg haloperidol (H), 10 mg/kg benztropine (B), 2.5 mg/kg H plus 10 mg/kg benztropine (H + B), or

[Influence of the intracaudate administration of kainic acid on the effects of the prolonged use of haloperidol and apomorphine on rats].

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In rats injected with kainic acid into the dorsal part of the caudate nucleus, the chronic treatment (for 20 days) with haloperidol (1 mg/kg) did not induce hypersensitivity of dopamine receptors. However, kainic acid produced no effect on hypersensitivity of the receptors after long-term

Bromocriptine-induced behavioral hypersensitivity: implications for the therapy of parkinsonism.

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Bromocriptine (CB-154) is a direct-acting dopamine agonist of proven clinical efficacy in parkinsonism. The capacity of bromocriptine to induce receptor site hypersensitivity was investigated utilizing a behavioral model in guinea pigs. Following 4 weeks of bromocriptine treatment, animals

Intrastriatal injection of kainic acid prevents the development of postsynaptic dopamine receptor hypersensitivity after chronic haloperidol treatment.

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Rats injected intrastriatally with kainic acid (KA), in contrast to sham-treated (control) animals, showed no tolerance toward catalepsy induced by chronic haloperidol treatment (28 days). After termination of chronic haloperidol treatment in control animals, apomorphine-induced stereotypy was

Chronic autoreceptor blockade and neuroleptic-induced dopamine receptor hypersensitivity.

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Metoclopramide and sulpiride, two benzamide compounds, are equally potent in terms of their ability to block postsynaptic D2 dopamine receptors. However these compounds show a marked divergence in their ability to block dopamine autoreceptors, as metoclopramide is 20-25-fold more potent than

Enhancement of hypophysectomy-induced dopamine receptor hypersensitivity in male rats by chronic haloperidol administration.

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It has been reported that hypophysectomy (HYPOX) would antagonize the development of a neuroleptic-induced dopamine receptor hypersensitivity, and suggested that the neuroleptic-induced dopamine receptor hypersensitivity may be mediated by the neuroleptic-induced hyperprolactinemia. Conversely, we

Neuroleptic-induced hypersensitivity of striatal dopamine receptors in the rat as a model of tardive dyskinesias. Effects of clozapine, haloperidol, loxapine and chlorpromazine.

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The present study has compared the abilities of clozapine, haloperidol, chlorpromazine and loxapine to induce dopamine (DA)-receptor hypersensitivity in rats, as measured by the apomorphine response after withdrawal of the antipsychotic drugs. Haloperidose during 1-2 weeks after withdrawal.

Difference in catalepsy response in inbred rats during chronic haloperidol treatment is not predictive of the intensity of behavioral hypersensitivity which subsequently develops.

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An animal model was utilized to explore the observed clinical association between a history of significant neuroleptic-induced parkinsonism and an increased incidence for the subsequent development of tardive dyskinesia. Catalepsy-sensitive Fisher rats and catalepsy-resistant Brown Norway rats were

Amantadine reduces haloperidol-induced dopamine receptor hypersensitivity in the striatum.

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In this report evidence is presented that amantadine hydrochloride greatly reduced the development of dopaminergic receptor hypersensitivity in the striatum, which normally results following chronic haloperidol administration using both a stereotyped behavior bioassay and a [3H]spiroperidol receptor

[Cutaneous necrosis at apomorphine injection points].

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BACKGROUND Apomorphine is a specific dopaminergic agonist used in the treatment of severe fluctuations of Parkinson's disease, particularly in patients on L-dopa. The drug is usually given subcutaneously, either as several daily injections or via a continuous subcutaneous delivery system. We

Effects of pretreatment with luteinizing hormone releasing hormone (LHRH) on behaviors induced by apomorphine in rats.

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The influence of LHRH on the behavioral effects induced by apomorphine (APO) was studied in male rats. Several doses of apomorphine (31.25, 62.5, 125, 250 and 500 micrograms/kg) were administered subcutaneously (SC) after LHRH 100 micrograms/kg or solvent. Low doses of apomorphine induced

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