Neuroleptic-induced striatal dopamine receptor supersensitivity in mice: Relationship to dose and drug

Ja, Severson; He, Robinson; Gm, Simpson

doi:10.1007/bf00432038

Cited by 26 publications

(7 citation statements)

References 30 publications

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“…7). The fact that acute and long-term haloperidol treatments did not significantly change the responsiveness of accumbens neurons to DA could appear most intriguing, given the well-documented supersensitivity of dopaminergic receptors after longterm neuroleptic treatments (Burt et al, 1977;Muller and Seeman, 1978;Skirboll and Bunney, 1979;Severson et al, 1984). However, several studies have reported that, contrary to microiontophoretic applications of haloperidol which antagonize DA-induced inhibition of caudate or accumbens neurons (Akaike et al, 1983(Akaike et al, , 1984, systemic administration of neuroleptics is ineffective in blocking the effects of microiontophoretic applications of DA (Ben-At-i and Kelly, 1976;Somjen et al, 1976;Zarzecki et al, 1977;Skirboll and Bunney, 1979;Johnson et al, 1986).…”

Section: Discussionmentioning

confidence: 99%

Effects of long-term haloperidol treatment on the responsiveness of accumbens neurons to cholecystokinin and dopamine: electrophysiological and radioligand binding studies in the rat

et al. 1990

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Cholecystokinin (CCK) and dopamine (DA) coexist in a subpopulation of neurons of the ventral tegmental area projecting to the nucleus accumbens. The present experiments were undertaken to determine the effect of acute and long-term administration of haloperidol on the responsiveness of accumbens neurons to microiontophoretic applications of the sulfated cholecystokinin octapeptide (CCK-8S), kainate (KA), and DA and on the density of CCK, D1, and D2 receptors determined by radioautography. Acute administration of haloperidol (1 mg/kg, i.v.) did not modify the neuronal responsiveness to DA and KA but increased that to CCK-8S. Long-term treatment with haloperidol decanoate (4 mg/kg/week, i.m., for 3-5 weeks) induced a marked increase in the responsiveness to CCK-8S, without noticeable change of that to DA and KA. After a 5 week treatment, significant increases in the amounts of CCK and D2 binding were found in the nucleus accumbens, whereas D1 binding parameters remained unchanged. Since long-term haloperidol treatment results in a depolarization inactivation of A10 dopaminergic neurons, these results suggest that, despite the reduced firing activity of mesolimbic dopaminergic neurons induced by the long-term haloperidol treatment, dopamine is still released in an amount sufficient to maintain a normal neuronal responsiveness of postsynaptic accumbens neurons to DA, whereas the release of CCK is possibly decreased to a greater extent, resulting in an enhanced responsiveness of the neurons to this peptide.

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Section: Discussionmentioning

confidence: 99%

Effects of long-term haloperidol treatment on the responsiveness of accumbens neurons to cholecystokinin and dopamine: electrophysiological and radioligand binding studies in the rat

et al. 1990

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“…Work in animal models shows that at equivalent doses and modes of treatment, long-term exposure to haloperidol produces dopamine receptor supersensitivity, while exposure to olanzapine or ziprasidone does not [10,12,156,175,176,177]. The two classes of antipsychotics have common but also different pharmacological properties.…”

Section: Choice Of the Antipsychoticmentioning

confidence: 99%

Antipsychotic-Induced Dopamine Supersensitivity Psychosis: Pharmacology, Criteria, and Therapy

Chouinard

Samaha

Chouinard

et al. 2017

Psychother Psychosom

225

227

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The first-line treatment for psychotic disorders remains antipsychotic drugs with receptor antagonist properties at D₂-like dopamine receptors. However, long-term administration of antipsychotics can upregulate D₂ receptors and produce receptor supersensitivity manifested by behavioral supersensitivity to dopamine stimulation in animals, and movement disorders and supersensitivity psychosis (SP) in patients. Antipsychotic-induced SP was first described as the emergence of psychotic symptoms with tardive dyskinesia (TD) and a fall in prolactin levels following drug discontinuation. In the era of first-generation antipsychotics, 4 clinical features characterized drug-induced SP: rapid relapse after drug discontinuation/dose reduction/switch of antipsychotics, tolerance to previously observed therapeutic effects, co-occurring TD, and psychotic exacerbation by life stressors. We review 3 recent studies on the prevalence rates of SP, and the link to treatment resistance and psychotic relapse in the era of second-generation antipsychotics (risperidone, paliperidone, perospirone, and long-acting injectable risperidone, olanzapine, quetiapine, and aripiprazole). These studies show that the prevalence rates of SP remain high in schizophrenia (30%) and higher (70%) in treatment-resistant schizophrenia. We then present neurobehavioral findings on antipsychotic-induced supersensitivity to dopamine from animal studies. Next, we propose criteria for SP, which describe psychotic symptoms and co-occurring movement disorders more precisely. Detection of mild/borderline drug-induced movement disorders permits early recognition of overblockade of D₂ receptors, responsible for SP and TD. Finally, we describe 3 antipsychotic withdrawal syndromes, similar to those seen with other CNS drugs, and we propose approaches to treat, potentially prevent, or temporarily manage SP.

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“…Overall, it appears that the chronic treatment of rats with CLOZ does not significantlyaltertheB,,,andKDofD2receptorsintherat striatum (Boysonetal., 1988;Jiangetal., 1990;Kusumietal., 1995;Lee and Tang, 1984;O'Dell et al, 1990;Rupniak et al, 1985;Seeget et al, 1982;Severson et al, 1984). A recent study has also shown that chronic CLOZ administration does not alter the density of striatal Dz receptors in mice (Zhang et al, 1995).…”

Section: Effect Of Chronic Cloz Administration On D Receptors In Thementioning

confidence: 86%

Pharmacological actions of the atypical antipsychotic drug clozapine: A review

Ashby

Wang

1996

Synapse

167

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Clozapine [8-chloro- 11-(4-methyl- 1-piperazinyl)-3H-dibenzo (b,e)(1,4) diazepine], or clozaril, is a member of the dibenazepine class of antipsychotic drugs. Initially, studies in animals using a number of neurochemical, biochemical, electrophysiological, and behavioral paradigms indicated that clozapine was markedly different from various typical antipsychotic drugs such as haloperidol and chlorpromazine. Subsequently, clinical studies have shown that clozapine is effective in ameliorating the core symptoms, as well as the negative symptoms, in schizophrenia. However, clozapine has a much lower propensity for inducing neurological side effects after acute or repeated administration compared to various typical neuroleptics. Furthermore, clozapine is therapeutically effective in treating about 30% of schizophrenic patients who are resistant to standard antipsychotic drugs. Based on the above information, clozapine has been designated an atypical antipsychotic drug. However, at this time, it is not entirely clear why clozapine is such a unique antipsychotic drug. To date, there has not been a comprehensive review regarding clozapine's pharmacological profile. Therefore, we will review clozapine's profile in the following areas: 1) affinity for neurotransmitter receptors in the brain; 2) electrophysiology (in vivo, single-cell recording and iontophoresis; in vitro studies); 3) in vivo microdialysis and voltammetry; 4) monoamine turnover or metabolism; 5) intermediate early gene expression; 6) positron emission tomography studies; and 7) molecular biological studies. We will also compare and contrast clozapine's acute and chronic effects, and discuss the merits of various hypotheses that have been put forward to explain clozapine's unique profile.

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Neuroleptic-induced striatal dopamine receptor supersensitivity in mice: Relationship to dose and drug

Cited by 26 publications

References 30 publications

Effects of long-term haloperidol treatment on the responsiveness of accumbens neurons to cholecystokinin and dopamine: electrophysiological and radioligand binding studies in the rat

Effects of long-term haloperidol treatment on the responsiveness of accumbens neurons to cholecystokinin and dopamine: electrophysiological and radioligand binding studies in the rat

Antipsychotic-Induced Dopamine Supersensitivity Psychosis: Pharmacology, Criteria, and Therapy

Pharmacological actions of the atypical antipsychotic drug clozapine: A review

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