Up-regulation of dopamine D2 receptor mRNA in rat striatum by chronic neuroleptic treatment

Rogue, P; Hanauer, André; Zwiller, Jean; Malviya, Anant N.; Vincendon, G.

doi:10.1016/0922-4106(91)90092-v

Cited by 53 publications

(19 citation statements)

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“…Other possible causes for the lack of consistency in the literature about the status of D3 receptor expression after chronic neuroleptic therapy include differences in drug dosage, treatment duration, or sensitivity of the assays employed. The notable resistance of the D3 dopamine receptor in the striatum to antagonist induced up-regulation contrasts the known increased D2 expression in this brain region resulting from chronic dopamine antagonist treatment (Fishburn et al, 1994;Rogue et al, 1991). Thus, if the EPS of chronic neuroleptic therapy is mediated through dopamine receptors in the motor striatum, D, or perhaps other dopamine receptors, rather than the D3 receptor, might be the culprit in the genesis of these undesirable motor complications.…”

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confidence: 92%

Up-regulation of D3 dopamine receptor mRNA by neuroleptics

Wang¹,

Hahn²,

Bishop³

et al. 1996

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The effects of 14 days neuroleptic treatment on the expression of the D3 dopamine receptor gene was investigated in rats using a sensitive polymerase chain reaction assay. In olfactory tubercle, D3 mRNA levels increased following haloperidol (40%), pimozide (56%), and sulpiride (63%) administration, and in nucleus accumbens, levels increased after haloperidol (50%) and sulpiride (50%). D3 expression in the motor striatum did not change with any antagonist tested. Clozapine did not affect D3 expression in any brain region. These data suggest that dopamine antagonists can regulate the expression of the D3 receptor in a brain region selective manner. The findings also suggest that the motor complications of chronic antipsychotic therapy are not due to D3 receptor up-regulation in the striatum.

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confidence: 92%

Up-regulation of D3 dopamine receptor mRNA by neuroleptics

Wang¹,

Hahn²,

Bishop³

et al. 1996

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“…In contrast, antipsychotics reduce internalization of D 2 receptors and produce an increase in brain D 2 receptor mRNA, a determinant of D 2 receptor density [66]. D 2 upregulation persists after discontinuation of antipsychotics [44] and produces alterations in intracellular systems, including G protein-coupled receptor kinase-6 (GRK-6) and β-arrestin 2, both of which are important for the internalization of D 2 receptors.…”

Section: Pharmacological Mechanisms By Which Antipsychotics Potentialmentioning

confidence: 99%

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

Chouinard

Samaha

Chouinard

et al. 2017

Psychother Psychosom

222

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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“…Administration of anti-psychotic drugs such as haloperidol to rats induces Zif268 expression in striatal neurons (Nguyen et al 1992;Simpson et al 1994), and haloperidol and sulpiride treatment induce increases in D2R mRNA in the rat striatum (Bernard et al 1991;Rogue et al 1991). We found that overexpression of Zif268 increased D2R promoter activity in a dose-dependent manner without an additive effect of MEKK cotransfection (Fig.…”

Section: Discussionmentioning

confidence: 54%

Activation of the rat dopamine D2 receptor promoter by mitogen‐activated protein kinase and Ca²⁺/calmodulin‐dependent protein kinase II pathways

Takeuchi¹,

Miyamoto²,

Fukunaga³

2002

Journal of Neurochemistry

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To investigate regulation of D2 receptor (D2R) gene expression by protein kinases, we evaluated effects of constitutively active MAPK kinase kinase (MEKK), Ca 2+ /calmodulindependent protein kinase (CaMK) II, CaMKIV and cyclic AMPdependent protein kinase (PKA) on D2R promoter activity using luciferase reporter gene assays. A 1.5-kbp fragment containing the rat D2R promoter was cloned upstream of the reporter and transfected into D2R-expressing NB2A cells or nonexpressing NG108-15 and C6 glioma cells. MEKK and CaMKII, but not CaMKIV and PKA, increased promoter activity 4.5-and 1.5-fold, respectively, in NB2A cells. Inhibitory effects of a MEK inhibitor and lack of effect by dominant negative (DN)-JNK1 or DN-p38MAPK revealed that ERK but not JNK and p38MAPK is involved in MEKK-induced promoter activation. Deletion and mutation of the promoter revealed that the MEKK-responsive region was Sp1 site B between nucleotides )56 and )47. Overexpression of Sp1 suppressed promoter activity without affecting MEKK-induced activation. Interestingly, overexpression of Zif268 increased promoter activity through the region between nucleotides )56 and )36. Increased activity by Zif268 was additive with CaMKII-induced activation but not with activation induced by MEKK. Co-transfection with CaMKII stimulated nuclear translocation of Zif268. These results suggest that ERK and CaMKII positively regulate the D2R promoter and that Zif268 is a potential transcription factor for the CaMKII-dependent pathway. Keywords: Ca 2+ /calmodulin-dependent protein kinase II, dopamine D2 receptor promoter, mitogen-activated protein kinase, NB2A cell, Zif268.

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Up-regulation of dopamine D2 receptor mRNA in rat striatum by chronic neuroleptic treatment

Cited by 53 publications

References 8 publications

Up-regulation of D3 dopamine receptor mRNA by neuroleptics

Up-regulation of D3 dopamine receptor mRNA by neuroleptics

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

Activation of the rat dopamine D2 receptor promoter by mitogen‐activated protein kinase and Ca²⁺/calmodulin‐dependent protein kinase II pathways

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Up-regulation of dopamine D2 receptor mRNA in rat striatum by chronic neuroleptic treatment

Cited by 53 publications

References 8 publications

Up-regulation of D3 dopamine receptor mRNA by neuroleptics

Up-regulation of D3 dopamine receptor mRNA by neuroleptics

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

Activation of the rat dopamine D2 receptor promoter by mitogen‐activated protein kinase and Ca2+/calmodulin‐dependent protein kinase II pathways

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Activation of the rat dopamine D2 receptor promoter by mitogen‐activated protein kinase and Ca²⁺/calmodulin‐dependent protein kinase II pathways