Haloperidol (but not ziprasidone) withdrawal enhances cocaine-induced locomotor activation and conditioned place preference in mice

Fukushiro, D.F.; Alvarez, Juliana do Nascimento; Tatsu, Julie Anne Obara; Castro, Juliana; Chinen, Cibele Cristina; Frussa‐Filho, Roberto

doi:10.1016/j.pnpbp.2007.01.025

Cited by 32 publications

(26 citation statements)

References 33 publications

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“…Conversely, atypical neuroleptics do not seem to produce the dopaminergic supersensitivity phenomenon, as suggested previously by earlier reports . Indeed, we have demonstrated that, in contrast with haloperidol, withdrawal from long‐term treatment with ziprasidone or risperidone does not modify the locomotor stimulant effect of cocaine and amphetamine in mice, respectively .…”

Section: Introductionsupporting

confidence: 84%

Effects of acute and long‐term typical or atypical neuroleptics on morphine‐induced behavioural effects in mice

Hollais

Patti

Zanin

et al. 2014

Clin Exp Pharma Physio

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1. It has been suggested that the high prevalence of drug abuse in schizophrenics is related to chronic treatment with typical neuroleptics and dopaminergic supersensitivity that develops as a consequence. Within this context, atypical neuroleptics do not seem to induce this phenomenon. In the present study, we investigated the effects of acute administration or withdrawal from long-term administration of haloperidol and/or ziprasidone on morphine-induced open-field behaviour in mice. 2. In the first experiment, mice were given a single injection of haloperidol (1 mg/kg, i.p.) or several doses of ziprasidone (2, 4 or 6 mg/kg, i.p.) and motor activity was quantified by the open-field test. The aim of the second experiment was to verify the effects of an acute injection of haloperidol (1 mg/kg) or ziprasidone (6 mg/kg) on 20 mg/kg morphine-induced behaviours in the open-field test. In the third experiment, mice were treated with 1 mg/kg haloperidol and/or 2, 4 or 6 mg/kg ziprasidone for 20 days. Seventy-two hours after the last injection, mice were injected with 20 mg/kg, i.p., morphine and then subjected to the open-field test. Acute haloperidol or ziprasidone decreased spontaneous general activity and abolished morphine-induced locomotor stimulation. 3. Withdrawal from haloperidol or ziprasidone did not modify morphine-elicited behaviours in the open-field test. The results suggest that withdrawal from neuroleptic treatments does not contribute to the acute effect of morphine in schizophrenic patients.

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Section: Introductionsupporting

confidence: 84%

Effects of acute and long‐term typical or atypical neuroleptics on morphine‐induced behavioural effects in mice

Hollais

Patti

Zanin

et al. 2014

Clin Exp Pharma Physio

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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

223

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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“…For example, schizophrenic patients have higher degrees of psychostimulant abuse (15–60%) than the general US population (Miller and Tanenbaum, 1989; Dixon et al, 1991; Volkow, 2009). While an increased rate of psychostimulant abuse may partly represent an attempt to overcome aversive symptoms or treatment-related side-effects (e.g., “self-medication” hypothesis) or an increased psychostimulant sensitivity due to “dopaminergic supersensitivity” induced by chronic antipsychotic treatment (Khantzian, 1985; Gawin and Kleber, 1986; LeDuc and Mittleman, 1995; Fukushiro et al, 2007), more recent studies have indicated potential mechanistic overlaps between psychostimulant abuse and other primary psychiatric disorders (see Volkow, 2009). Psychostimulants, especially the amphetamine derivatives, may induce psychotic states in mentally ill or vulnerable individuals (Connell, 1958; Ellinwood, 1968; Angrist and Gershon, 1970; Janowsky and Risch, 1979; Mahoney et al, 2008), and they may adversely affect the clinical course of psychiatric disorders (Janowsky and Davis, 1974; Drake and Wallach, 1989; Glasner-Edwards et al, 2010).…”

Section: Psychostimulant Addictionmentioning

confidence: 99%

Pharmacologically-mediated reactivation and reconsolidation blockade of the psychostimulant-abuse circuit: A novel treatment strategy

Lee

Szabo

Fowler

et al. 2012

Drug and Alcohol Dependence

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Psychostimulant abuse continues to present legal, socioeconomic and medical challenges as a primary psychiatric disorder, and represents a significant comorbid factor in major psychiatric and medical illnesses. To date, monotherapeutic drug treatments have not proven effective in promoting long-term abstinence in psychostimulant abusers. In contrast to clinical trials utilizing monotherapies, combinations of dopamine (DA) agonists and selective 5-HT3, 5HT2A/2C, or NK1 antagonists have shown robust efficacy in reversing behavioral and neurobiological alterations in animal models of psychostimulant abuse. One important temporal requirement for these treatments is that the 5-HT or NK1 receptor antagonist be given at a critical time window after DA agonist administration. This requirement may reflect a necessary dosing regimen towards normalizing underlying dysfunctional neural circuits and “addiction memory” states. Indeed, chronic psychostimulant abuse can be conceptualized as a consolidated form of dysfunctional memory maintained by repeated drug- or cue-induced reactivation of neural circuit and subsequent reconsolidation. According to this concept, the DA agonist given first may reactivate this memory circuit, thereby rendering it transiently labile. The subsequent antagonist is hypothesized to disrupt reconsolidation necessary for restabilization, thus leading progressively to a therapeutically-mediated abolishment of dysfunctional synaptic plasticity. We propose that long-term abstinence in psychostimulant abusers may be achieved not only by targeting putative mechanistic pathways, but also by optimizing drug treatment regimens designed to disrupt the neural processes underlying the addicted state.

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Haloperidol (but not ziprasidone) withdrawal enhances cocaine-induced locomotor activation and conditioned place preference in mice

Cited by 32 publications

References 33 publications

Effects of acute and long‐term typical or atypical neuroleptics on morphine‐induced behavioural effects in mice

Effects of acute and long‐term typical or atypical neuroleptics on morphine‐induced behavioural effects in mice

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

Pharmacologically-mediated reactivation and reconsolidation blockade of the psychostimulant-abuse circuit: A novel treatment strategy

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