Effects of melatonin on behavioral dopaminergic supersensitivity

Abı́lio, Vanessa C.; Vera, João A.R; Ferreira, Leonardo S.M; Duarte, Carlo R.M; Martins, César; Torres-Leite, Danila; Ribeiro, R. de A.; Frussa‐Filho, Roberto

doi:10.1016/s0024-3205(03)00231-5

Cited by 27 publications

(7 citation statements)

References 54 publications

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“…As already mentioned previously, it is important to highlight that although withdrawal from long‐term haloperidol treatment was ineffective at modifying morphine‐induced hyperlocomotion, it may have produced the development of the dopaminergic supersensitivity phenomenon. Indeed, long‐term treatment with conventional neuroleptics, such as haloperidol, produces a compensatory increment of both the number and the affinity of dopamine D2 receptors and, consequently, behavioural supersensitivity to dopamine agonists . Conversely, the atypical neuroleptics (risperidone and ziprasidone) do not seem to induce the dopaminergic supersensitivity phenomenon …”

Section: Discussionmentioning

confidence: 99%

“…Indeed, long-term treatment with conventional neuroleptics, such as haloperidol, produces a compensatory increment of both the number 5,31 and the affinity 32,33 of dopamine D2 receptors and, consequently, behavioural supersensitivity to dopamine agonists. [34][35][36][37] Conversely, the atypical neuroleptics (risperidone and ziprasidone) do not seem to induce the dopaminergic supersensitivity phenomenon. 16 We have shown previously that withdrawal from haloperidol treatment increases the locomotor stimulation induced by the psychostimulant agents cocaine 14,15 and amphetamine.…”

Section: Discussionmentioning

confidence: 99%

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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: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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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“…Locomotor activity ( Abilio et al, 2003b ) was assessed in a circular open-field arena (97 cm in diameter and 32.5 cm high, with an open top and a floor divided into 19 similar quadrants). The animals were individually placed on the apparatus.…”

Section: Methodsmentioning

confidence: 99%

Cannabidiol Prevents Motor and Cognitive Impairments Induced by Reserpine in Rats

et al. 2016

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Cannabidiol (CBD) is a non-psychotomimetic compound from Cannabis sativa that presents antipsychotic, anxiolytic, anti-inflammatory, and neuroprotective effects. In Parkinson’s disease patients, CBD is able to attenuate the psychotic symptoms induced by L-DOPA and to improve quality of life. Repeated administration of reserpine in rodents induces motor impairments that are accompanied by cognitive deficits, and has been applied to model both tardive dyskinesia and Parkinson’s disease. The present study investigated whether CBD administration would attenuate reserpine-induced motor and cognitive impairments in rats. Male Wistar rats received four injections of CBD (0.5 or 5 mg/kg) or vehicle (days 2–5). On days 3 and 5, animals received also one injection of 1 mg/kg reserpine or vehicle. Locomotor activity, vacuous chewing movements, and catalepsy were assessed from day 1 to day 7. On days 8 and 9, we evaluated animals’ performance on the plus-maze discriminative avoidance task, for learning/memory assessment. CBD (0.5 and 5 mg/kg) attenuated the increase in catalepsy behavior and in oral movements – but not the decrease in locomotion – induced by reserpine. CBD (0.5 mg/kg) also ameliorated the reserpine-induced memory deficit in the discriminative avoidance task. Our data show that CBD is able to attenuate motor and cognitive impairments induced by reserpine, suggesting the use of this compound in the pharmacotherapy of Parkinson’s disease and tardive dyskinesia.

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“…The hypothesis of hypersensitivity of dopamine receptors secondary to chronic dopamine receptor blockade by antipsychotics is one of the most popular models, as reflected by the number of genetic studies investigating dopamine system genes. [22][23][24][25][26] This hypothesis is based on several observations. Antipsychotic treatment results in persistent dyskinesia in non-human primates, with significantly decreased dopamine turnover in the caudate and substantia nigra.…”

Section: And Tarsy Andmentioning

confidence: 99%

Association study of tardive dyskinesia and five DRD4 polymorphisms in schizophrenia patients

Zai

Tiwari²,

Basile³

et al. 2009

Pharmacogenomics J

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Tardive dyskinesia (TD) is a side effect of chronic antipsychotic medication exposure. Abnormalities in dopaminergic activity in the nigro-striatal system have been most often suggested to be involved because the agents that cause TD share in common potent antagonism of dopamine D(2) receptors (DRD2). Thus, a number of studies have focused on the association of dopamine system gene polymorphisms and TD, with the most consistent findings being an association between TD and the Ser9Gly polymorphism of the DRD3 gene and the TaqIA site 3' of the DRD2 gene. The DRD4 gene codes for the third member of the D(2)-like dopamine receptor family, and the variable number tandem-repeat polymorphism in exon 3 of DRD4 has been associated with TD. However, other polymorphisms have not been thoroughly examined. In this study, we investigated five polymorphisms spanning the DRD4 gene and their association with TD in our European Caucasian sample (N=171). Although the exon 3 variable number tandem repeat was not associated with TD, haplotypes consisting of four tag polymorphisms were associated with TD in males. This study suggests that DRD4 may be involved in TD in the Caucasian population, although further replication studies are needed.

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Effects of melatonin on behavioral dopaminergic supersensitivity

Cited by 27 publications

References 54 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

Cannabidiol Prevents Motor and Cognitive Impairments Induced by Reserpine in Rats

Association study of tardive dyskinesia and five DRD4 polymorphisms in schizophrenia patients

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