Amphetamine induction of c-fos in the nucleus accumbens is not inhibited by glutamate antagonists

Dalia, Asad; Wallace, Lane J.

doi:10.1016/0006-8993(95)00794-q

Cited by 23 publications

(13 citation statements)

References 26 publications

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“…Together, these data suggest that generalized disruption of motor function most likely did not contribute to decreased reinstatement. These findings are in agreement with previous data on the effects of these drugs on locomotion (Dalia and Wallace, 1995;Bristow et al, 1996;Mead and Stephens, 1999;Ossowska et al, 2001). Measurement of spontaneous locomotor activity may, however, have only limited value as control of drug-induced changes in reinstatement behavior, because habituated animals have relatively low basal activity levels.…”

Section: Discussionsupporting

confidence: 92%

Ionotropic and Metabotropic Glutamate Receptor Antagonism Attenuates Cue-Induced Cocaine Seeking

Bäckström

Hyytiä

2005

Neuropsychopharmacol

161

121

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Neuroanatomical and pharmacological evidence implicates glutamate transmission in drug-environment conditioning that partly controls drug seeking and relapse. Glutamate receptors could be targets for pharmacological attenuation of the motivational properties of drugpaired cues and for relapse prevention. The purpose of the present study was therefore to investigate the involvement of ionotropic and metabotropic glutamate receptor subtypes in cue-induced reinstatement of cocaine-seeking behavior. Rats were trained to selfadminister cocaine using a second-order schedule of reinforcement (FR4(FR5:S)) under which a compound stimulus (light and tone) associated with cocaine infusions was presented contingently. Following extinction, the effects of the competitive NMDA receptor antagonist CGP 39551 (0, 2.5, 5, 10 mg/kg intraperitoneally (i.p.)), two competitive AMPA/kainate antagonists, CNQX (0, 0.75, 1.5, 3 mg/ kg i.p.) and NBQX (0, 1.25, 2.5, 5 mg/kg i.p.), the NMDA/glycine site antagonist L-701,324 (0, 0.63, 1.25, 2.5 mg/kg i.p.), and the mGluR5 antagonist MPEP (0, 1.25, 2.5, 5 mg/kg i.p.) on cue-induced reinstatement of cocaine seeking were examined. The AMPA/kainate receptor antagonists CNQX and NBQX, the NMDA/glycine site antagonist L-701,324, and the mGluR5 antagonist MPEP attenuated significantly cue-induced reinstatement. The NMDA antagonist CGP 39551 failed to affect reinstatement. Additional control experiments indicated that attenuation of cue-induced reinstatement by CNQX, NBQX, L-701,324, and MPEP was not accompanied by significant suppression of spontaneous locomotor activity. These results suggest that conditioned influences on cocaine seeking depend on glutamate transmission. Accordingly, drugs with antagonist properties at various glutamate receptor subtypes could be useful in prevention of relapse induced by conditioned stimuli.

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Section: Discussionsupporting

confidence: 92%

Ionotropic and Metabotropic Glutamate Receptor Antagonism Attenuates Cue-Induced Cocaine Seeking

Bäckström

Hyytiä

2005

Neuropsychopharmacol

161

121

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“…They also suggest that the activation of the corticostriatal pathway is critical for the stimulatory effects of cocaine, as its ability to induce c-fos expression is diminished in mice with reduced NMDA receptor expression. Although dopamine-and amphetamine-stimulated c-fos expression in the striatum is also affected by NMDA receptor-mediated glutamatergic signaling from the frontal cortex (Konradi et al, 1996;Cenci and Björklund, 1993;Badiani et al, 1998), our results are in line with reports suggesting that amphetamine c-fos induction might be less sensitive to decreased NMDA receptor function (Dalia and Wallace, 1995;Morelli, 1997;Ganguly and Keefe, 2000;Miyamoto S et al, 2004).…”

Section: Biochemical Measures Of Postsynaptic Response To Psychostimusupporting

confidence: 92%

Genetic NMDA Receptor Deficiency Disrupts Acute and Chronic Effects of Cocaine but not Amphetamine

Ramsey

Laakso

Cyr

et al. 2008

Neuropsychopharmacol

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NMDA receptor-mediated glutamate transmission is required for several forms of neuronal plasticity. Its role in the neuronal responses to addictive drugs is an ongoing subject of investigation. We report here that the acute locomotor-stimulating effect of cocaine is absent in NMDA receptor-deficient mice (NR1-KD). In contrast, their acute responses to amphetamine and to direct dopamine receptor agonists are not significantly altered. The striking attenuation of cocaine's acute effects is not likely explained by alterations in the dopaminergic system of NR1-KD mice, since most parameters of pre-and postsynaptic dopamine function are unchanged. Consistent with the behavioral findings, cocaine induces less c-Fos expression in the striatum of these mice, while amphetamine-induced c-Fos expression is intact. Furthermore, chronic cocaine-induced sensitization and conditioned place preference are attenuated and develop more slowly in mutant animals, but amphetamine's effects are not altered significantly. Our results highlight the importance of NMDA receptor-mediated glutamatergic transmission specifically in cocaine actions, and support a hypothesis that cocaine and amphetamine elicit their effects through differential actions on signaling pathways.

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“…First, we demonstrate that a conditioned motor response with this behavioral paradigm was context-specific, results that are consistent with other studies (Ahmed et al, 1995;Badiani et al, 1995;Jodogne et al, 1994;Shen et al, 2006;Tirelli & Terry, 1998). Secondly, non-contingent AMPH administration activated Fos in all brain regions examined except the VP, results that are consistent with other studies (Cadoni et al, 1995;Dalia & Wallace, 1995;Engber et al, 1998;Niles et al, 1997). Thirdly, AMPH administered in the context that reliably predicted AMPH (i.e., the AMPH-paired context) activated Fos in the hippocampus, BLA, NAcC, NAcS, and DLS.…”

Section: Discussionsupporting

confidence: 81%

Context modulates the expression of conditioned motor sensitization, cellular activation and synaptophysin immunoreactivity

Rademacher

Napier

Meredith

2007

Eur J of Neuroscience

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We tested the hypothesis that amphetamine-(AMPH) induced conditioned motor sensitization is accompanied by cellular activation (measured by Fos immunoreactivity) and synaptophysin immunoreactivity in reward-related brain areas. Forty-eight rats were tested for conditioned motor sensitization using a conditioning paradigm that was performed in a three-chambered apparatus. Rats underwent two drug pairings with 1.0 mg/kg AMPH in one outer chamber and, on alternate days, were paired with saline in the other. On the fifth day, relative to the first AMPH treatment, AMPH administration increased motor activity in the AMPH-paired context but not in the saline-paired context. Relative to the first saline treatment, saline on the fifth day produced a conditioned increase in motor activity when given in the chamber previously paired with AMPH, and saline given in the saline-paired context produced a conditioned decrease in motor activity. AMPH administered in the AMPH-paired context increased the density of both Fos and synaptophysin immunoreactivity in the dentate gyrus, cornu ammonis (CA)1, CA3, basolateral amygdala, and dorsolateral striatum. This pairing between context and drug increased Fos but not synaptophysin immunoreactivity in the nucleus accumbens core and shell. Saline administered in the AMPH-paired context increased the density of Fos immunoreactivity in the basolateral amygdala and nucleus accumbens core. These data indicate that the basolateral amygdala-nucleus accumbens core pathway is necessary for the context-elicited conditioned motor responses, while the hippocampus encodes the spatial context.

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Amphetamine induction of c-fos in the nucleus accumbens is not inhibited by glutamate antagonists

Cited by 23 publications

References 26 publications

Ionotropic and Metabotropic Glutamate Receptor Antagonism Attenuates Cue-Induced Cocaine Seeking

Ionotropic and Metabotropic Glutamate Receptor Antagonism Attenuates Cue-Induced Cocaine Seeking

Genetic NMDA Receptor Deficiency Disrupts Acute and Chronic Effects of Cocaine but not Amphetamine

Context modulates the expression of conditioned motor sensitization, cellular activation and synaptophysin immunoreactivity

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