The synergistic effect of fluoxetine on the locomotor hyperactivity induced by MK-801, a non-competitive NMDA receptor antagonist

J, Maj; Rogóż, Z; Skuza, G; Wędzony, K

doi:10.1007/bf01292622

Cited by 25 publications

(17 citation statements)

References 39 publications

(45 reference statements)

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“…The results of the present study stand in contrast to those previously reported by Callaway et al (1990) and Maj et al (1996), who found that fluoxetine did not affect the locomotor response to amphetamine. However, in those studies fluoxetine was administered 60 and 120 min, respectively, before the amphetamine treatment while in the present study fluoxetine was administered 30 min prior to treatment with amphetamine.…”

Section: Figcontrasting

confidence: 86%

Acute fluoxetine treatment potentiates amphetamine hyperactivity and amphetamine-induced nucleus accumbens dopamine release: possible pharmacokinetic interaction

et al. 1999

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Amphetamine stimulates locomotor activity, in large part by activating central dopaminergic systems. Serotonin shares on overlapping distribution with dopamine and has been shown to modulate dopaminergic function and dopamine-mediated behaviors. The present study examined whether increasing serotonergic function, via the selective serotonin reuptake inhibitor fluoxetine, would alter the stimulatory effects of amphetamine on locomotor activity and dopamine overflow in the nucleus accumbens. In addition, the present study determined whether fluoxetine treatment would alter the metabolism of amphetamine. Results show that 5.0 mg/kg fluoxetine potentiated the locomotor activity induced by amphetamine (0.5-1.0 mg/ kg), and enhanced the increased dopamine overflow in the nucleus accumbens induced by amphetamine. Fluoxetine treatment also resulted in a higher concentration of amphetamine in the CNS. Together, these findings indicate that acute fluoxetine treatment potentiates the locomotor stimulating and dopamine activating effects of amphetamine. Further, the results indicate that fluoxetine potentiates the effects of amphetamine by decreasing the metabolism of amphetamine, probably through inhibition of cytochrome P450 isozymes.

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Section: Figcontrasting

confidence: 86%

Acute fluoxetine treatment potentiates amphetamine hyperactivity and amphetamine-induced nucleus accumbens dopamine release: possible pharmacokinetic interaction

et al. 1999

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“…It is noteworthy that some experiments failed to observe an interaction between MK-801 and WAY 100135 at a level of locomotor activity (Maj et al 1996). This discrepancy may result from two facts.…”

Section: Locomotor Activitymentioning

confidence: 41%

“…This discrepancy may result from two facts. First, the effect of WAY 100135, however strong, is transient and may be obscured by the potent long-lasting stimulatory effect of MK-801, especially when results are presented in a cumulative manner (Maj et al 1996). Secondly, in the present study we used an experimental procedure which differentiated between locomotion and stereotyped behavior ȩ ȩ concomitant with locomotor hyperactivity, the latter being unaffected by WAY 100135.…”

Section: Locomotor Activitymentioning

confidence: 99%

WAY 100135, an Antagonist of 5-HT1A Serotonin Receptors, Attenuates Psychotomimetic Effects of MK-801

Wędzony

Maćkowiak

Zaja̧czkowski

et al. 2000

Neuropsychopharmacology

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Non-competitive antagonists of NMDA receptors such as phencyclidine (PCP) or ketamine are known for their strong, frequently neuroleptic-resistant psychotomimetic effects in humans (Javitt and Zukin 1991). These clinical effects, as well as evidence suggesting the involvement of NMDA receptors in the pathophysiology of schizophrenia (Carlsson et al. 1999;Harrison 1999;Wachtel and Turski 1990), support the experimental modeling of psychoses by administration of non-competitive NMDA receptor antagonists (Jentsch and Roth 1999). In this respect, MK-801 seems to be of special interest in experimental pharmacology. It belongs to a class of non-competitive NMDA receptor antagonists (Seeburg 1993;Lodge and Johnson 1990; Willetts et al. 1990) and MK-801 seems to be highly specific to the PCP binding site located in the ion channel of the NMDA receptor complex (Lodge and Johnson 1990;Seeburg 1993 (Carlsson 1993;Maj et al. 1991), impairment of sensorimotor gating (Mansbach and Geyer 1989; W dzony et al. 1994), and detrimental effects on spatial working memory (Verma and Moghaddam 1996). Although it is generally agreed that the psychostimulant and psychotomimetic effects of PCP, ketamine, and MK-801 are initiated by blockade of the NMDA receptor ion channel complex, the neuronal pathways or neurotransmitter systems involved in the propagation of the psychotomimetic effects are not precisely known (Bakshi and Geyer 1998). Moreover, the apparent lack of chemical compounds which might directly abolish the pharmacological blockade of these NMDA receptors (Lodge and Johnson 1990; Willetts et al. 1990), and prevent impairments of their function during the course of schizophrenia (Harrison 1999) justifies attempts to define neuroanatomical/neurochemical systems responsible for the propagation of the effects of non-competitive NMDA receptors.Apart from the dopaminergic system (Jentsch and Roth 1999), traditionally linked with psychotomimetic effects of non-competitive antagonists of NMDA receptors, and the noradrenergic system [currently under investigation (Bakshi and Geyer 1998, 1999;Jentsch et al. 1998)], considerable interest has been focused on serotonin and its receptors (Geyer 1998). It has been shown, for example, that MK-801 increases serotonin release (Whitton et al. 1992) and influences serotonin turnover (Loscher et al. 1991;W dzony et al. 1997). Moreover, the psychostimulant and psychotomimetic effects of MK-801 and PCP are attenuated by specific antagonists of 5-HT2A receptors (Schmidt and Fadayel 1996;Varty et al. 1999;Varty and Higgins 1995).Apart from 5-HT2A receptors, a growing number of studies indicate that MK-801 may also influence other serotonin receptors; for example, it increases mRNA of 5-HT6 and 5-HT7 receptors (Healy and Meador-Woodruff 1999). Moreover, the increased density of 5-HT1A receptors after a single administration of MK-801 has been reported in one of our recent studies (W dzony et al. 1997). The possible involvement of 5-HT1A receptors in the psychotomimetic effects of NMDA receptor antagon...

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“…However, since Willins et al (1992) found that 1 g/side of DNQX decreased the locomotor response to 0.5 mg/kg AMPH, it may be that DNQX has unique effects on METH stimulated behavior. Serotonin releasing agents have been shown to synergistically enhance the locomotor activating properties of GLU antagonists (Maj et al 1996). METH is known to be more effective at releasing serotonin than AMPH .…”

Section: Discussionmentioning

confidence: 99%

Neurochemical and behavioral differences between d-methamphetamine and d-amphetamine in rats

et al. 2003

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The synergistic effect of fluoxetine on the locomotor hyperactivity induced by MK-801, a non-competitive NMDA receptor antagonist

Cited by 25 publications

References 39 publications

Acute fluoxetine treatment potentiates amphetamine hyperactivity and amphetamine-induced nucleus accumbens dopamine release: possible pharmacokinetic interaction

Acute fluoxetine treatment potentiates amphetamine hyperactivity and amphetamine-induced nucleus accumbens dopamine release: possible pharmacokinetic interaction

WAY 100135, an Antagonist of 5-HT1A Serotonin Receptors, Attenuates Psychotomimetic Effects of MK-801

Neurochemical and behavioral differences between d-methamphetamine and d-amphetamine in rats

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