Effects of acute and chronic antidepressant administration on phencyclidine (PCP) induced locomotor hyperactivity

Redmond, A. M.; Harkin, Andrew; Kelly, John; Leonard, Brian E.

doi:10.1016/s0924-977x(98)00023-6

Cited by 29 publications

(17 citation statements)

References 32 publications

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“…The hypothesis that NMDA antagonists are effective antidepressants was based on the observation that interfering with NMDA [49,50] . Multiple NMDA receptor antagonists were reported to mimic the effects of antidepressants in more complex models, including chronic mild stress and olfactory bulbectomy [51][52][53] . This clinical and preclinical evidence linked major depressive disorder to dysregulated glutamate neurotransmission.…”

Section: Discussionmentioning

confidence: 99%

Timosaponin derivative YY-23 acts as a non-competitive NMDA receptor antagonist and exerts a rapid antidepressant-like effect in mice

Zhang

Guo

et al. 2015

Acta Pharmacol Sin

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Aim: N-methyl-D-aspartic acid (NMDA) receptor modulators have shown promising results as potential antidepressant agents, whereas timosaponins extracted from the Chinese herb Rhizoma Anemarrhenae exhibit antidepressant activities. In the present study we examined whether YY-23, a modified metabolite of timosaponin B-III, could affect NMDA receptors in rat hippocampal neurons in vitro, and evaluated its antidepressant-like effects in stressed mice. Methods: NMDA-induced currents were recorded in acutely dissociated rat hippocampal CA1 neurons using a whole-cell recording technique. C57BL/6 mice were exposed to a 6-week chronic mild stress (CMS) or a 10-d chronic social defeat stress (CSDS). The stressed mice were treated with YY-23 (20 mg·kg -1 ·d -1 ) or a positive-control drug, fluoxetine (10 mg·kg -1 ·d -1 ) for 3 weeks. Behavioral assessments were carried out every week. Results: In acutely dissociated rat hippocampal CA1 neurons, YY-23 selectively and reversibly inhibited NMDA-induced currents with an EC 50 value of 2.8 μmol/L. This inhibition of NMDA-induced currents by YY-23 was non-competitive, and had no features of voltagedependency or use-dependency. Treatment of the stressed mice with YY-23 not only reversed CMS-induced deficiency of sucrose preference and immobility time, and CSDS-induced reduction of social interaction, but also had faster onset as compared to fluoxetine. Conclusion: YY-23 is a novel non-competitive antagonist of NMDA receptors with promising rapid antidepressant-like effects in mouse models of CMS and CSDS depression.

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Section: Discussionmentioning

confidence: 99%

Timosaponin derivative YY-23 acts as a non-competitive NMDA receptor antagonist and exerts a rapid antidepressant-like effect in mice

Zhang

Guo

et al. 2015

Acta Pharmacol Sin

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“…Acute fluoxetine or citalopram increases amphetamine-induced hyperlocomotion Millan et al, 2003) but has no effect on phencyclidine-induced model (Redmond et al, 1999). Repeated fluoxetine or citalopram treatment tends to enhance amphetamine-induced hyperlocomotion (Arnt et al, 1984;Sills et al, 1999Sills et al, , 2000 and phencyclidine-induced hyperlocomotion (Redmond et al, 1999). Taken together, a combination of repeated amphetamine and phencyclidine hyperlocomotion models may be utilized to distinguish anxiolytics and antidepressants from antipsychotics.…”

Section: Acknowledgementsmentioning

confidence: 99%

“…Interestingly, antidepressants such as fluoxetine and citalopram also exhibit a behavioral profile distinctive from that of antipsychotics. Acute fluoxetine or citalopram increases amphetamine-induced hyperlocomotion Millan et al, 2003) but has no effect on phencyclidine-induced model (Redmond et al, 1999). Repeated fluoxetine or citalopram treatment tends to enhance amphetamine-induced hyperlocomotion (Arnt et al, 1984;Sills et al, 1999Sills et al, , 2000 and phencyclidine-induced hyperlocomotion (Redmond et al, 1999).…”

Section: Acknowledgementsmentioning

confidence: 99%

Repeated antipsychotic treatment progressively potentiates inhibition on phencyclidine-induced hyperlocomotion, but attenuates inhibition on amphetamine-induced hyperlocomotion: Relevance to animal models of antipsychotic drugs

Sun

2009

European Journal of Pharmacology

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“…chlordiazepoxide) nor antidepressant treatment (eg. fluoxetine and citalopram) progressively potentiates their inhibition of PCP-induced hyperlocomotion across sessions and prolongs this action within sessions [24,32,40]. When the long-term effects are assessed in a subsequent challenge test, adult rats previously treated with olanzapine show an enhanced response to olanzapine (i.e.…”

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confidence: 99%

Is Brain-derived Neurotrophic Factor a Possible Mechanism Underlying Risperidone Sensitization in Adolescent Rats?

Shu¹

2013

Biochem & Pharmacol

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IntroductionBrain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family that is widely distributed in the brain with the highest levels found in the hippocampus and other cortical areas [1]. It is involved in many functional processes critical for the brain development and experience-dependent neuroplasticity, such as neuronal survival, neural migration, differentiation, synapse formation, and modulation of neurotransmitter synthesis [2][3][4]. It also plays an important role in stress response, learning and memory, and actions of psychoactive drugs [5][6][7]. Accumulating clinical evidence indicates that abnormal BDNF expressions may contribute to pathophysiology of schizophrenia, as the levels of BDNF have been found decreased in peripheral (blood) and central (brain) systems of patients with schizophrenia [8][9][10][11]. Antipsychotic drugs can also alter the brain levels of BDNF, and prevent the stress-induced decrease in the levels of BDNF, indicating that it may also regulate the action of antipsychotic drugs [12][13][14][15][16][17].In recent years, we have used the Conditioned Avoidance Response (CAR) and phencyclidine (PCP)-induced hyperlocomotion to examine the long-term treatment effects of antipsychotic drugs [18][19][20][21][22][23]. Both tests are known for their high predictive validity for antipsychotic efficacy, as antipsychotic drugs show a robust suppression of avoidance response and PCP-induced hyperlocomotion upon acute drug administration [24,25]. Testing an antipsychotic drug in two independent tests of antipsychotic activity is necessary to ensure that any observed antipsychotic effect is not an artifact of any particular model but reflects the generality of the treatment effect. We have been particularly interested in how repeated antipsychotic treatment alters this suppression over time. Such alterations can be manifested as either tolerance, which is characterized by decreased responsiveness to a certain drug effect, or sensitization, which is characterized by increased responsiveness to a drug effect [26]. The typical paradigm that we developed to study antipsychotic sensitization and tolerance consists of an induction phase, in which rats are repeatedly treated with an antipsychotic drug or vehicle for several days and tested for their avoidance responses and PCP-induced hyperlocomotion, and an expression phase, in which all rats are given a challenge dose of the drug and their avoidance and motor activity under PCP is tested again [18,19,21,22,27]. Using such a paradigm, we show that repeated treatment of haloperidol or olanzapine progressively increases its suppression of avoidance responding across the test sessions in the induction phase, and makes animals more sensitive to these drugs AbstractRisperidone is one of the most widely used atypical antipsychotic drugs and is approved for the treatment of mental disorders (eg. schizophrenia, autism) in children and adolescents. The present study investigated the repeated treatment effect of risperidone and associa...

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Effects of acute and chronic antidepressant administration on phencyclidine (PCP) induced locomotor hyperactivity

Cited by 29 publications

References 32 publications

Timosaponin derivative YY-23 acts as a non-competitive NMDA receptor antagonist and exerts a rapid antidepressant-like effect in mice

Timosaponin derivative YY-23 acts as a non-competitive NMDA receptor antagonist and exerts a rapid antidepressant-like effect in mice

Repeated antipsychotic treatment progressively potentiates inhibition on phencyclidine-induced hyperlocomotion, but attenuates inhibition on amphetamine-induced hyperlocomotion: Relevance to animal models of antipsychotic drugs

Is Brain-derived Neurotrophic Factor a Possible Mechanism Underlying Risperidone Sensitization in Adolescent Rats?

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