Electroconvulsive shock prevents dopamine receptor supersensitivity

Lerer, Bernard; Jabotinsky-Rubin, K; Bannet, Jacob; Ebstein, Richard P.; Belmaker, Robert H.

doi:10.1016/0014-2999(82)90188-1

Cited by 20 publications

(4 citation statements)

References 10 publications

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“…7 ' 8,9 ' l0 ' 29,3a31 This benefit was not however, confirmed by Ward et al 32 Moreover in rats, ECT prevents haloperidol induced dopamine receptor hypersensitivity. 33 These conflicting data are difficult to reconcile with our observations and raise the possibility that, in dopaminomimetic psychosis, ECT may be producing its effect via non-dopaminergic mechanisms.…”

Section: Discussioncontrasting

confidence: 68%

Treatment of Dopaminomimetic Psychosis in Parkinson's Disease with Electroconvulsive Therapy

Hurwitz

Calne

Waterman

1988

Can. j. neurol. sci.

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Section: Discussioncontrasting

confidence: 68%

Treatment of Dopaminomimetic Psychosis in Parkinson's Disease with Electroconvulsive Therapy

Hurwitz

Calne

Waterman

1988

Can. j. neurol. sci.

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“…The increase is similar to that induced by nigrostriatal lesions [7]. In animal models, increased D 2 density is associated with behavioral supersensitivity to dopamine stimulation manifested by TD-like symptoms [42,43], increased psychomotor activity in response to the dopamine agonists amphetamine and apomorphine [44,45,46], decreased efficacy in models of antipsychotic-like effects [9,10], and increased pursuit of reward cues in response to amphetamine [11,12,13]. Many of the older animal studies showing that chronic antipsychotic treatment produces dopamine D 2 receptor upregulation have used very high doses of antipsychotic/D 2 receptor occupancy.…”

Section: Pharmacological Mechanisms By Which Antipsychotics Potentialmentioning

confidence: 69%

“…Usually, a rebound psychosis or transient SP can appear rapidly [33]. As for ECT, it can transiently increase striatal dopamine release [196] and attenuate both haloperidol-induced increases in D 2 receptor density and behavioral supersensitivity to the dopamine agonist apomorphine [45]. As mentioned above, the link between changes in D 2 receptor number/function and SP remains to be determined.…”

Section: Guidelines For Sp Treatmentmentioning

confidence: 99%

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

Chouinard

Samaha

Chouinard

et al. 2017

Psychother Psychosom

216

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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“…Both investigators are of the opinion, therefore, that electroshock activates the nigrostriatal dopamine system as an indirect result of current spread rather than via the seizure per se. All the same, it is well known that electroconvulsive shock enhances dopamine agonist behaviours (Bhavsar et al, 1981; but see Lerer et al, 1982), more especially those mediated by dopamine D, receptors (Sharp et al, 1990). Confusingly, electroshock has been variously reported as decreasing D, receptor binding in the limbic forebrain (De Montis et al, 1990) and either increasing D, receptor turnover in the striatum (Nowak and Zak, 1989) or not affecting striatal dopamine receptors (Bergstrom and Kellar, 1979;Deakin et al, 1981).…”

Section: Electrically Induced Seizuresmentioning

confidence: 99%

The role of dopamine in epilepsy

Starr

1996

Synapse

239

157

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The clinical benefits of dopamine agonists in the management of epilepsy can be traced back over a century, whilst the introduction of neuroleptics into psychiatry practice 40 years ago witnessed the emergence of fits as a side effect of dopamine receptor blockade. Epidemiologists noticed a reciprocal relationship between the supposed dopaminergic overactivity syndrome of schizophrenia and epilepsy, which came to be regarded as a dopamine underactivity condition. Early pharmacological studies of epilepsy employed nonselective drugs, that often did not permit dopamine's antiepileptic action to be clearly dissociated from that of other monoamines. Likewise, the biochemical search for genetic abnormalities in brain dopamine function, as predeterminants of spontaneous epilepsy, proved largely inconclusive. The discovery of multiple dopamine receptor families (D1 and D2), mediating opposing influences on neuronal excitability, heralded a new era of dopamine‐epilepsy research. The traditional anticonvulsant action of dopamine was attributed to D2 receptor stimulation in the forebrain, while the advent of selective D1 agonists with proconvulsant properties revealed for the first time that dopamine could also lower the seizure threshold from the midbrain. Whilst there is no immediate prospect of developing D2 agonists or D1 antagonists as clinically useful antiepileptics, there is a growing awareness that seizures might be precipitated as a consequence of treating other neurological disorders with D2 antagonists (schizophrenia) or D1 agonists (parkinsonism). © 1996 Wiley‐Liss, Inc.

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Electroconvulsive shock prevents dopamine receptor supersensitivity

Cited by 20 publications

References 10 publications

Treatment of Dopaminomimetic Psychosis in Parkinson's Disease with Electroconvulsive Therapy

Treatment of Dopaminomimetic Psychosis in Parkinson's Disease with Electroconvulsive Therapy

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

The role of dopamine in epilepsy

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