Mechanisms of Action of Antipsychotic Drugs of Different Classes, Refractoriness to Therapeutic Effects of Classical Neuroleptics, and Individual Variation in Sensitivity to their Actions: PART II

Miller, Robert J.

doi:10.2174/157015909790031184

Cited by 51 publications

(25 citation statements)

References 114 publications

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“…Taken together with the present data, we suggest that the role of D 1 in drug effects to disrupt and potentially improve salience allocation merits further investigation. It has been suggested that D 1 antagonism may be important for the behavioral effects of antipsychotics and may be secondary to D 2 antagonism (Josselyn et al , 1997; Miller, 1990, 2009). A potential role for D 1 in AMP disruption of LI is consistent with studies in rats implicating D 1 in overshadowing, a related measure of salience allocation, other behavioral effects of AMP in other species, as well as a more general role for midbrain D 1 in attentional accuracy (Liu et al , 2010, 2011; O'Tuathaigh and Moran, 2002; Zelikowsky and Fanselow, 2010).…”

Section: Discussionmentioning

confidence: 99%

D-Amphetamine and Antipsychotic Drug Effects on Latent Inhibition in Mice Lacking Dopamine D2 Receptors

Bay-Richter

O'Callaghan

Mathur

et al. 2013

Neuropsychopharmacol

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Drugs that induce psychosis, such as 𝒟-amphetamine (AMP), and those that alleviate it, such as antipsychotics, are suggested to exert behavioral effects via dopamine receptor D2 (D2). All antipsychotic drugs are D2 antagonists, but D2 antagonism underlies the severe and debilitating side effects of these drugs; it is therefore important to know whether D2 is necessary for their behavioral effects. Using D2-null mice (Drd2−/−), we first investigated whether D2 is required for AMP disruption of latent inhibition (LI). LI is a process of learning to ignore irrelevant stimuli. Disruption of LI by AMP models impaired attention and abnormal salience allocation consequent to dysregulated dopamine relevant to schizophrenia. AMP disruption of LI was seen in both wild-type (WT) and Drd2−/−. This was in contrast to AMP-induced locomotor hyperactivity, which was reduced in Drd2−/−. AMP disruption of LI was attenuated in mice lacking dopamine receptor D1 (Drd1−/−), suggesting that D1 may play a role in AMP disruption of LI. Further supporting this possibility, we found that D1 antagonist SKF83566 attenuated AMP disruption of LI in WT. Remarkably, both haloperidol and clozapine attenuated AMP disruption of LI in Drd2−/−. This demonstrates that antipsychotic drugs can attenuate AMP disruption of learning to ignore irrelevant stimuli in the absence of D2 receptors. Data suggest that D2 is not essential either for AMP to disrupt or for antipsychotic drugs to reverse AMP disruption of learning to ignore irrelevant stimuli and further that D1 merits investigation in the mediation of AMP disruption of these processes.

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Section: Discussionmentioning

confidence: 99%

D-Amphetamine and Antipsychotic Drug Effects on Latent Inhibition in Mice Lacking Dopamine D2 Receptors

Bay-Richter

O'Callaghan

Mathur

et al. 2013

Neuropsychopharmacol

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“…[2] Therapeutic efficacy of atypical antipsychotics varies from drug to drug in different individuals. [3] Risperidone is one of the well-established SGA and widely used in the treatment of schizophrenia. [4] It has a combined antagonist effects for dopamine ( DRD2 ) and serotonin ( 5HTR2A , 2C ) receptors.…”

Section: Introductionmentioning

confidence: 99%

Risperidone-Induced Adverse Drug Reactions and Role of DRD2 (−141 C Ins/Del) and 5HTR2C (−759 C>T) Genetic Polymorphisms in Patients with Schizophrenia

Alladi

Mohan

Shewade

et al. 2017

Journal of Pharmacology and Pharmacotherapeutics

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Objective:To determine the adverse drug reaction (ADR) profile of risperidone and their association with dopamine (DRD2 − 141 C Ins/Del/rs1799732) and serotonin receptor (5HTR2C −759 C>T/rs3813929) gene polymorphisms in patients with schizophrenia.Materials and Methods:The study was conducted among 289 patients who were diagnosed with schizophrenia and were on treatment with risperidone (4–8 mg/day)-based therapy for a minimum of 4 weeks. Genotyping was carried by real-time quantitative polymerase chain reaction. All the patients were observed for the occurrences of ADRs during the study. Changes in prolactin levels and body weight were analyzed for a subgroup of 102 and 97 patients, respectively.Results:Risperidone-induced extrapyramidal symptoms (EPSs) were seen in 36.7% of patients. Among them, tremors were the most common symptom 31.8%. Risperidone-induced hyperprolactinemia and weight gain were seen in 87.2% and 53.6% in subgroup patients. Adverse effects such as sedation, gastrointestinal effects, and amenorrhea were seen in 9.7% (28/289), 5.1% (15/289), and 6.1% (7/114), respectively. Occurrence of DRD2 − 141 Ins/Del and Del/Del polymorphisms were significantly associated with increased prolactin levels in response to risperidone (odds ratio [OR] = 10.45; 95% confidence interval = 1.29–84.89, P = 0.004). No such association was observed with 5HTR2C (−759 C>T) polymorphism. Weight gain and EPS were not associated with the above genetic polymorphisms.Conclusion:Hyperprolactinemia, weight gain, and EPSs (>36.7%) were common adverse effects of risperidone. DRD2 – 141C Ins/Del and Del/Del polymorphisms were significantly associated with increased prolactin levels (OR = 10.45) in response to risperidone.

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“…If clozapine is re-introduced to treat the withdrawal psychosis, the dose Barnes et al 593 required to achieve remission may be substantially higher than that initially prescribed (Miodownik et al, 2006). While the mechanism of such 'rebound psychosis' remains unclear, attributions have been made to supersensitivity of mesolimbic dopamine receptor sites and specific properties of clozapine (Alphs and Lee, 1991;Miller, 2009;Shiovitz et al, 1996;Tanrı´verdi and Yazı´cı´, 1996).…”

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confidence: 99%

Evidence-based guidelines for the pharmacological treatment of schizophrenia: recommendations from the British Association for Psychopharmacology

2011

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These guidelines from the British Association for Psychopharmacology address the scope and targets of pharmacological treatment for schizophrenia. A consensus meeting, involving experts in schizophrenia and its treatment, reviewed key areas and considered the strength of evidence and clinical implications. The guidelines were drawn up after extensive feedback from the participants and interested parties, and cover the pharmacological management and treatment of schizophrenia across the various stages of the illness, including first-episode, relapse prevention, and illness that has proved refractory to standard treatment. The practice recommendations presented are based on the available evidence to date, and seek to clarify which interventions are of proven benefit. It is hoped that the recommendations will help to inform clinical decision making for practitioners, and perhaps also serve as a source of information for patients and carers. They are accompanied by a more detailed qualitative review of the available evidence. The strength of supporting evidence for each recommendation is rated.

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Mechanisms of Action of Antipsychotic Drugs of Different Classes, Refractoriness to Therapeutic Effects of Classical Neuroleptics, and Individual Variation in Sensitivity to their Actions: PART II

Cited by 51 publications

References 114 publications

D-Amphetamine and Antipsychotic Drug Effects on Latent Inhibition in Mice Lacking Dopamine D2 Receptors

D-Amphetamine and Antipsychotic Drug Effects on Latent Inhibition in Mice Lacking Dopamine D2 Receptors

Risperidone-Induced Adverse Drug Reactions and Role of DRD2 (−141 C Ins/Del) and 5HTR2C (−759 C>T) Genetic Polymorphisms in Patients with Schizophrenia

Evidence-based guidelines for the pharmacological treatment of schizophrenia: recommendations from the British Association for Psychopharmacology

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