Differential regulation of dopamine receptors after chronic typical and atypical antipsychotic drug treatment

Tarazi, Frank I.; Florijn, Wouter J.; Creese, Ian

doi:10.1016/s0306-4522(96)00631-8

Cited by 95 publications

(52 citation statements)

References 60 publications

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“…This result confirmed previous reports that both short-term and chronic olanzapine treatment did not affect D 2 R bindings in the PFC, CPu and NAc (Kusumi et al, 2000, Han et al, 2009a. Similarly it has been reported that SGAs with lower affinity to D 2 R such as clozapine and quetiapine did not affect D 2 R bindings, while antipsychotics with high D 2 R affinity such as haloperidol, chlorpromazine and risperidone have been reported to increase D 2 R bindings (Tarazi et al, 1997, Kusumi et al, 2000, Tarazi et al, 2001). These results are consistent with a PET study showing that olanzapine had a lower D 2 R blockade compared to haloperidol in schizophrenia patients (Xiberas et al, 2001).…”

Section: Discussionsupporting

confidence: 91%

Effects of olanzapine and betahistine co-treatment on serotonin transporter, 5-HT2A and dopamine D2 receptor binding density

Lian

Huang

Pai

et al. 2013

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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. 2013, 'Effects of olanzapine and betahistine co-treatment on serotonin transporter, 5-HT2A and dopamine D2 receptor binding density ', vol. 47, Effects of olanzapine and betahistine co-treatment on serotonin transporter, 5-HT2A and dopamine D2 receptor binding density AbstractOlanzapine is widely used in treating multiple domains of schizophrenia symptoms but induces serious metabolic side-effects. Recent evidence has showed that co-treatment of betahistine (a histaminergic H1 receptor agonist and H3 receptor antagonist) is effective for preventing olanzapine-induced weight gain/ obesity, however it is not clear whether this co-treatment affects on the primary therapeutic receptor binding sites of olanzapine such as serotonergic 5-HT2A receptors (5-HT2AR) and dopaminergic D2 receptors (D2R). Therefore, this study investigated the effects of this co-treatment on 5-HT2AR, 5-HT transporter

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Section: Discussionsupporting

confidence: 91%

Effects of olanzapine and betahistine co-treatment on serotonin transporter, 5-HT2A and dopamine D2 receptor binding density

Lian

Huang

Pai

et al. 2013

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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“…However, chronic administration of APs is known to alter the regional density of several neurotransmitter receptors in the central nervous system, including those for dopamine, serotonin, acetylcholine, histamine, and glutamate, that may contribute to the observed proconvulsant effects of some antipsychotics [42,53,54]. These changes, in particular upregulation of dopamine receptors, have been suggested as the basis for some of the adverse effects that occur with long-term antipsychotic therapy [55]. The effects of APs and their known affinities for several receptor subtypes are listed in Table 2.…”

Section: General Considerations On the Effect Of Aps On Seizuresmentioning

confidence: 99%

Comparative Analysis of the Treatment of Chronic Antipsychotic Drugs on Epileptic Susceptibility in Genetically Epilepsy-prone Rats

et al. 2015

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Antipsychotic drugs (APs) are of great benefit in several psychiatric disorders, but they can be associated with various adverse effects, including seizures. To investigate the effects of chronic antipsychotic treatment on seizure susceptibility in genetically epilepsy-prone rats, some APs were administered for 7 weeks, and seizure susceptibility (audiogenic seizures) was evaluated once a week during treatment and for 5 weeks after drug withdrawal. Furthermore, acute and subchronic (5-day treatment) effects were also measured. Rats received haloperidol (0.2-1.0 mg/kg), clozapine (1-5 mg/kg), risperidone (0.03-0.50 mg/kg), quetiapine (2-10 mg/kg), aripriprazole (0.2-1.0 mg/kg), and olanzapine (0.13-0.66 mg/kg), and tested according to treatment duration. Acute administration of APs had no effect on seizures, whereas, after regular treatment, aripiprazole reduced seizure severity; haloperidol had no effects and all other APs increased seizure severity. In chronically treated rats, clozapine showed the most marked proconvulsant effects, followed by risperidone and olanzapine. Quetiapine and haloperidol had only modest effects, and aripiprazole was anticonvulsant. Finally, the proconvulsant effects lasted at least 2-3 weeks after treatment suspension; for aripiprazole, a proconvulsant rebound effect was observed. Taken together, these results indicate and confirm that APs might have the potential to increase the severity of audiogenic seizures but that aripiprazole may exert anticonvulsant effects. The use of APs in patients, particularly in patients with epilepsy, should be monitored for seizure occurrence, including during the time after cessation of therapy. Further studies will determine whether aripiprazole really has a potential as an anticonvulsant drug and might also be clinically relevant for epileptic patients with psychiatric comorbidities.

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“…Short treatment periods of rats with clozapine has been reported not to increase striatal D 2 -like receptor levels. 45,48 This suggests that the upregulation of striatal D 2 -like receptors is more likely associated with drug-induced extrapyramidal motor side effects rather than mediation of their antipsychotic action.…”

Section: Dovepressmentioning

confidence: 99%

A correlation of haloperidol-induced cognitive deficit with dysfunctional dopamine receptor activity in nonhuman primate

Navarro‐Lobato¹,

Masmudi‐Martín²,

López‐Aranda³

et al. 2010

OAAP

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Abstract:Haloperidol is an antipsychotic drug that acts through blockage of dopamine D 2 receptors. Chronic administration of this antipsychotic drug in nonhuman primates induces a pronounced cognitive deficit. However, receptor subtypes that are responsible for this cognitive dysfunction remain unknown. Therefore, brains of chronic haloperidol-treated young and aged monkeys were used to analyze the intricate relation of receptor activity, cognitive dysfunction, and haloperidol-mediated actions in the production of harmful effects. Taking into account the significant cognitive loss observed after haloperidol treatment, it was predicted that changes in the cognitive status that correlate with the receptor activity in the prefrontal cortex and striatum, areas implicated in the processing of haloperidol-mediated effects in brain, should be common in both young and aged animals. Based on this concept, we observed that in the prefrontal cortex, dopamine D 1 and D 2 receptors showed changes in receptor levels that were common in both age groups. However, this relationship was absent in GABA A , serotonin 5HT2 and muscaranic receptors. In contrast to the prefrontal cortex, in striatum, this change was restricted to the dopamine D 2 receptors only. Therefore, from our results, it seems that apart from the downregulation of D 1 receptor activity in the prefrontal cortex, an upregulation of D 2 receptors could also contribute to the generation of the cognitive loss observed in haloperidol-treated monkeys. Additionally, reduced excitatory input due to hampered cortico-striatal D 1 dopaminergic activity and stronger inhibition at the synapse of excitatory input site by upregulated striatal D 2 receptor activity could promote the side effects associated with haloperidol.

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Differential regulation of dopamine receptors after chronic typical and atypical antipsychotic drug treatment

Cited by 95 publications

References 60 publications

Effects of olanzapine and betahistine co-treatment on serotonin transporter, 5-HT2A and dopamine D2 receptor binding density

Effects of olanzapine and betahistine co-treatment on serotonin transporter, 5-HT2A and dopamine D2 receptor binding density

Comparative Analysis of the Treatment of Chronic Antipsychotic Drugs on Epileptic Susceptibility in Genetically Epilepsy-prone Rats

A correlation of haloperidol-induced cognitive deficit with dysfunctional dopamine receptor activity in nonhuman primate

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