Competitive and noncompetitive NMDA antagonists block sensitization to methamphetamine

Ohmori, Tetsuro; Abekawa, Tomohiro; Muraki, Akira; Koyama, Tsukasa

doi:10.1016/0091-3057(94)90318-2

Cited by 97 publications

(44 citation statements)

References 33 publications

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“…After a recovery period of 10 days, the rats were infused with 3 μg flesinoxan or saline 10 min before testing. Their motor activity in Plexiglas boxes (38×33×17 cm) was recorded as described by Ohmori et al (1994) automatically for 5 min by electronic digital counters with infrared cell sensors between 0800 and 1300 h. Horizontal movement was digitized and fed into a computer.…”

Section: Motor Activitymentioning

confidence: 99%

5-HT1A receptor agonist affects fear conditioning through stimulations of the postsynaptic 5-HT1A receptors in the hippocampus and amygdala

Inoue

Abekawa

et al. 2006

European Journal of Pharmacology

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Evidence from preclinical and clinical studies has shown that 5-HT 1A receptor agonists have anxiolytic actions. The anxiolytic actions of 5-HT 1A receptor agonists have been tested by our previous studies using fear conditioning. However, little is known about the brain regions of anxiolytic actions of 5-HT 1A receptor agonists in this paradigm. In the present study, we investigated the effects of bilateral microinjections of flesinoxan, a selective 5-HT 1A receptor agonist, into the hippocampus, amygdala and medial prefrontal cortex on the expression of contextual conditioned freezing and the defecation induced by conditioned fear stress in rats. These results reveal that both intrahippocampal and intraamygdala injections of flesinoxan decreased the expression of conditioned freezing, while injections into the medial prefrontal cortex did not. In addition, intraamygdala injection of flesinoxan attenuated the increased defecation induced by conditioned fear, but injections into the hippocampus and medial prefrontal cortex failed. These results suggest that flesinoxan exerts its anxiolytic actions in the fear conditioning through stimulations of the postsynaptic 5-HT 1A receptors in the hippocampus and amygdala.

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Section: Motor Activitymentioning

confidence: 99%

5-HT1A receptor agonist affects fear conditioning through stimulations of the postsynaptic 5-HT1A receptors in the hippocampus and amygdala

Inoue

Abekawa

et al. 2006

European Journal of Pharmacology

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“…Glutamate receptor antagonists, as well as excitotoxic lesions of the prefrontal cortex (PFC), can block the development of behavioral sensitization to psychostimulants (Karler et al, 1989(Karler et al, , 1994Wolf and Khansa, 1991;Kalivas and Alesdatter, 1993;Schenk et al, 1993;Stewart and Druhan, 1993;Wolf and Jeziorski, 1993;Ohmori et al, 1994;Wolf et al, 1995;Cador et al, 1999). Moreover, release of glutamate in the NAc and VTA is enhanced in amphetamine-sensitized rats (Xue et al, 1996;Wolf andXue, 1998, 1999;Wolf et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Expression of Amphetamine-Induced Behavioral Sensitization after Short- and Long-Term Withdrawal Periods: Participation of μ- and δ-Opioid Receptors

Magendzo

Bustos

2002

Neuropsychopharmacol

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Repeated amphetamine administration results in behavioral sensitization, an enduring behavioral transformation expressed after short and long periods of withdrawal. To investigate the participation of the opioid system in amphetamine-induced behavioral sensitization, we studied the effect of naloxone, an opioid receptor antagonist, on the expression of behavioral sensitization tested after short-(2 days) and long-term (14 days) withdrawal periods. In addition, using quantitative competitive RT-PCR, we examined the levels of m-opioid receptor (MOR) and d-opioid receptor (DOR) mRNA in the nucleus accumbens shell (NAcSh) and ventral tegmental area (VTA) of behaviorally sensitized rats, at these two withdrawal times. This study showed that whereas naloxone did not modify the expression of behavioral sensitization tested after 2 days of withdrawal, it completely blocked the expression when tested after 14 days of withdrawal. DOR and MOR mRNA levels were not modified in the NAcSh of rats expressing behavioral sensitization after 2 or 14 days of withdrawal. Conversely, DOR and MOR mRNA levels were elevated in the VTA of animals expressing behavioral sensitization after 2 days of withdrawal. However, whereas DOR mRNA returned to control levels, MOR mRNA levels remained elevated in animals expressing behavioral sensitization after 14 days of withdrawal. These results indicate a striking difference between the role played by opioid receptors in the expression of amphetamine-induced behavioral sensitization, when tested after short-or long-term withdrawal periods. In addition, our results support the notion that repeated amphetamine-induced changes in opioid receptor expression may contribute to the perpetuation of psychostimulant abuse and/or relapse.

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“…A few studies have used cleaner, competitive NMDAR antagonists in examining psychostimulant-induced sensitization [45,46,17,20,27,29,41,[47][48][49][50][51][52][53][54]. For example, Wolf et al [27] used CGS19755 and found a "clean block" of amphetamine sensitization -i.e., stereotyped and locomotor behavior did not increase with repeated administration in rats co-administered CGS19755 with amphetamine.…”

Section: Introductionmentioning

confidence: 99%

“…Co-administration of MK801 prevents the development of sensitization to cocaine [15][16][17][18][19][20][21][22][23], amphetamine [24][25][26][27][28] and methamphetamine [29,30]. Moreover, MK801 similarly prevents the development of cocaine, amphetamine, and methamphetamineinduced conditioned place preference, a prominent associative memory model of drug seeking behavior [31][32][33].…”

Section: Introductionmentioning

confidence: 99%

The competitive NMDA receptor antagonist CPP disrupts cocaine-induced conditioned place preference, but spares behavioral sensitization

Carmack

Kim²,

Sage³

et al. 2013

Behavioural Brain Research

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h i g h l i g h t sCPP co-administration with cocaine altered the acute response to cocaine. NMDAR antagonism with CPP had no effect on cocaine-induced behavioral sensitization. NMDAR antagonism with CPP abolished cocaine-induced conditioned place preference. a r t i c l e i n f o a b s t r a c tRecently, the notion that memory and addiction share similar neural substrates has become widely accepted. N-methyl-d-aspartate receptors (NMDAR) are the cornerstones of synaptic models of memory. The present study examined the effect of the competitive NMDAR antagonist CPP on the induction of behavioral sensitization and conditioned place preference to cocaine. Conditioned place preference is an associative memory model of drug seeking, while sensitization is a non-associative model of the transition from casual to compulsive use. There were three principal findings: (1) co-administration of CPP and cocaine altered the acute response to cocaine, suggesting a direct interaction between the two drugs; (2) NMDAR antagonism had no effect on behavioral sensitization; and (3) NMDAR antagonism abolished conditioned place preference. A review of prior evidence supporting a role for NMDARs in sensitization suggests that NMDAR antagonists directly interfere with cocaine's psychostimulant effects, and this interaction could be misinterpreted as a disruption of sensitization. Finally, we suggest that addiction recruits multiple kinds of plasticity, with sensitization recruiting NMDAR-independent mechanisms.

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Competitive and noncompetitive NMDA antagonists block sensitization to methamphetamine

Cited by 97 publications

References 33 publications

5-HT1A receptor agonist affects fear conditioning through stimulations of the postsynaptic 5-HT1A receptors in the hippocampus and amygdala

5-HT1A receptor agonist affects fear conditioning through stimulations of the postsynaptic 5-HT1A receptors in the hippocampus and amygdala

Expression of Amphetamine-Induced Behavioral Sensitization after Short- and Long-Term Withdrawal Periods: Participation of μ- and δ-Opioid Receptors

The competitive NMDA receptor antagonist CPP disrupts cocaine-induced conditioned place preference, but spares behavioral sensitization

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