Effects of quetiapine on phencyclidine-induced cognitive deficits in mice: A possible role of α1-adrenoceptors

Tanibuchi, Yuko; Fujita, Yūkō; Kohno, Masashi; Ishima, Tamaki; Takatsu, Yuto; Iyo, Masaomi; Hashimoto, Kenji

doi:10.1016/j.euroneuro.2009.07.005

Cited by 34 publications

(29 citation statements)

References 48 publications

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“…9,25 Interestingly, the observation on quetiapine, which is an antipsychotic agent, can be analogous to that of chloropromazine, attributing the effects of both medications to a1-adrenergic antagonism. 22,34 Moreover, hypertension was another positively associated factor with IFIS, a finding that has been also emerged at previous studies 31 and our previous metaanalysis on the field. 16 Of note, duration of any of the medications was not found to be associated with IFIS.…”

Section: Discussionsupporting

confidence: 58%

Risk factors for intraoperative floppy iris syndrome: a prospective study

Chatziralli

Peponis

Parikakis

et al. 2016

Eye

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Section: Discussionsupporting

confidence: 58%

Risk factors for intraoperative floppy iris syndrome: a prospective study

Chatziralli

Peponis

Parikakis

et al. 2016

Eye

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“…Another atypical antipsychotic drug, lurasidone, also produces a dose-dependent reversal of the effect of subchronic PCP on NOR (Horiguchi and Meltzer, unpublished data). Quetiapine and aripiprazole, two other atypical antipsychotic drugs, also reverse the effect of a subchronic PCP regimen on NOR in rodents (Nagai et al, 2009;Tanibuchi et al, 2009). The ability of eight atypical antipsychotic drugs, which are 5-HT 2A antagonists, to reverse the effects of subchronic PCP suggests that this may be a general property of atypical antipsychotic drugs that achieve 5-HT 2A and D 2 receptor blockade.…”

Section: Discussionmentioning

confidence: 96%

Attenuation of Phencyclidine-Induced Object Recognition Deficits by the Combination of Atypical Antipsychotic Drugs and Pimavanserin (ACP 103), a 5-Hydroxytryptamine_2A Receptor Inverse Agonist

Snigdha

Horiguchi

Huang

et al. 2009

J Pharmacol Exp Ther

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Subchronic administration of the N-methyl-D-aspartate receptor antagonist, phencyclidine (PCP), in rodents has been shown to produce impairment in novel object recognition (NOR), a model of visual learning and memory. We tested the hypothesis that the selective 5-HT 2A inverse agonists, pimavanserin and, would potentiate subeffective doses of atypical antipsychotic drugs (APDs) to reverse the NOR deficits. Female rats received vehicle or PCP (2 mg/kg b.i.d.) for 7 days, followed by a 7-day washout. Pimavanserin (3 mg/kg) or M100907 (1 mg/kg) alone, or four atypicial APDs, risperidone (0.05-0.1 mg/kg), melperone (1-3 mg/kg), olanzapine (1-2 mg/kg), or N-desmethylclozapine (1-2 mg/kg), and the typical APD, haloperidol (0.05-0.1 mg/kg), were administered alone, or in combination with pimavanserin or M100907, before NOR testing. The exploration times of objects during 3-min acquisition and retention trials, separated by a 1-min interval, were compared by analysis of variance. Vehicle-, but not PCP-treated, animals, explored the novel object significantly more than the familiar in the retention trial (p Ͻ 0.05-0.01). Pretreatment with the higher doses of the atypical APDs, but not pimavanserin, M100907, or haloperidol alone, reversed the effects of PCP. The effect of risperidone was blocked by haloperidol pretreatment. Coadministration of pimavanserin or M100907, with ineffective doses of the atypical APDs, but not haloperidol, also reversed the PCP-induced deficit in NOR. These results support the importance of 5-hydroxytryptamine 2A receptor blockade relative to D 2 receptor blockade in the ability of atypicals to ameliorate the effect of subchronic PCP, a putative measure of cognitive dysfunction in schizophrenia.

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“…This could also help explain our finding that M 1 function in pyramidal neurons remains intact in the PFC of the PCP-treated mice. Indeed, there is evidence that shows that both acute and repeated NMDA receptor antagonism can lead to a marked loss in GABAergic neurotransmission in the brain including the frontal cortex (Brigman et al, 2009;Jentsch et al, 1998;Tanibuchi et al, 2009). For instance, loss of LTD at the hippocampo-PFC synapse has been postulated to be due to a failure in the recruitment of GABAergic interneurons in the PFC by the hippocampal inputs following repeated PCP treatment (Thomases et al, 2014).…”

Section: Role Of M 1 Pam In Pcp-treated Micementioning

confidence: 99%

Potentiation of M1 Muscarinic Receptor Reverses Plasticity Deficits and Negative and Cognitive Symptoms in a Schizophrenia Mouse Model

Ghoshal

Rook

Dickerson

et al. 2015

Neuropsychopharmacol

122

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Schizophrenia patients exhibit deficits in signaling of the M 1 subtype of muscarinic acetylcholine receptor (mAChR) in the prefrontal cortex (PFC) and also display impaired cortical long-term depression (LTD). We report that selective activation of the M 1 mAChR subtype induces LTD in PFC and that this response is completely lost after repeated administration of phencyclidine (PCP), a mouse model of schizophrenia. Furthermore, discovery of a novel, systemically active M 1 positive allosteric modulator (PAM), VU0453595, allowed us to evaluate the impact of selective potentiation of M 1 on induction of LTD and behavioral deficits in PCP-treated mice. Interestingly, VU0453595 fully restored impaired LTD as well as deficits in cognitive function and social interaction in these mice. These results provide critical new insights into synaptic changes that may contribute to behavioral deficits in this mouse model and support a role for selective M 1 PAMs as a novel approach for the treatment of schizophrenia.

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Effects of quetiapine on phencyclidine-induced cognitive deficits in mice: A possible role of α1-adrenoceptors

Cited by 34 publications

References 48 publications

Risk factors for intraoperative floppy iris syndrome: a prospective study

Risk factors for intraoperative floppy iris syndrome: a prospective study

Attenuation of Phencyclidine-Induced Object Recognition Deficits by the Combination of Atypical Antipsychotic Drugs and Pimavanserin (ACP 103), a 5-Hydroxytryptamine_2A Receptor Inverse Agonist

Potentiation of M1 Muscarinic Receptor Reverses Plasticity Deficits and Negative and Cognitive Symptoms in a Schizophrenia Mouse Model

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Effects of quetiapine on phencyclidine-induced cognitive deficits in mice: A possible role of α1-adrenoceptors

Cited by 34 publications

References 48 publications

Risk factors for intraoperative floppy iris syndrome: a prospective study

Risk factors for intraoperative floppy iris syndrome: a prospective study

Attenuation of Phencyclidine-Induced Object Recognition Deficits by the Combination of Atypical Antipsychotic Drugs and Pimavanserin (ACP 103), a 5-Hydroxytryptamine2A Receptor Inverse Agonist

Potentiation of M1 Muscarinic Receptor Reverses Plasticity Deficits and Negative and Cognitive Symptoms in a Schizophrenia Mouse Model

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Product

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Attenuation of Phencyclidine-Induced Object Recognition Deficits by the Combination of Atypical Antipsychotic Drugs and Pimavanserin (ACP 103), a 5-Hydroxytryptamine_2A Receptor Inverse Agonist