A Single<i>In Vivo</i>Exposure to Cocaine Abolishes Endocannabinoid-Mediated Long-Term Depression in the Nucleus Accumbens

Fourgeaud, Lawrence; Mato, Susana; Bouchet, Delphine; Hémar, Agnès; Worley, Paul F.; Manzoni, Olivier J.

doi:10.1523/jneurosci.0671-04.2004

Cited by 188 publications

(214 citation statements)

References 39 publications

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“…The changes in short-term plasticity observed in our study contrast several studies that did not observe significant changes in the paired-pulse ratio in mice that were either treated with or self-administered cocaine (Thomas et al, 2001;Fourgeaud et al, 2004;SchrammSapyta et al, 2006). This disparity most likely reflects differences between the pharmacological effects of cocaine and amphetamine.…”

Section: Discussioncontrasting

confidence: 97%

“…This is consistent with the finding that chronic cocaine administration produces an enhanced sensitivity to DA (Beurrier and Malenka, 2002). In addition, other investigators have found that presynaptic inhibition by endocannabinoids is unaffected by a single systemic injection of cocaine (Fourgeaud et al, 2004). Thus, presynaptic KOP receptor modulation of glutamate release in the NAc appears to be selectively lost following exposure to psychostimulants.…”

Section: Discussionsupporting

confidence: 89%

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Acute Amphetamine Exposure Selectively Desensitizes κ-Opioid Receptors in the Nucleus Accumbens

Xia

Whistler

et al. 2007

Neuropsychopharmacol

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In the present study, we investigated the effects of psychostimulant exposure on k-opioid peptide (KOP) receptor signaling in the rat mesolimbic system. A single subcutaneous (s.c.) injection of amphetamine (2.5 mg/kg) reduced the KOP receptor-mediated inhibition of glutamate release in the nucleus accumbens shell, as a consequence of KOP receptor desensitization. This effect was blocked by dopamine (DA) receptor antagonists or the nonselective opioid antagonist, naltrexone (1 mg/kg, s.c.), and mimicked by the KOP receptor agonists U69593 (0.32 mg/kg, s.c.) and dynorphin (1 mM), indicating that an amphetamine-induced release of dynorphin is producing a long-lasting desensitization of the KOP receptor. Despite the fact that amphetamine also increases dynorphin release in the ventral tegmental area (VTA), KOP receptor function in this region was not affected by amphetamine; there was no difference in the KOP receptor-mediated change in firing rate or resting membrane potential measured in VTA neurons from saline-or amphetaminetreated animals. This study demonstrates that amphetamine can produce regionally selective adaptations in KOP receptor signaling, which may, in turn, alter the effects of subsequent drug exposure.

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Section: Discussioncontrasting

confidence: 97%

Section: Discussionsupporting

confidence: 89%

Acute Amphetamine Exposure Selectively Desensitizes κ-Opioid Receptors in the Nucleus Accumbens

Xia

Whistler

et al. 2007

Neuropsychopharmacol

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“…injection of either 0.9% saline or 30mg/kg cocaine, put back in their home cages and then sacrificed either 45 minutes or 24 hours later. These time points were chosen based on previous studies that showed glutamate levels peak at approximately 40 minutes following acute cocaine (Smith et al, 1995;Reid et al, 1997) and changes in mGluR5 expression 24 hours following a cocaine exposure (Fourgeaud et al, 2004).…”

Section: Experimental Procedures Animals and Cocaine Treatmentsmentioning

confidence: 99%

“…A single in vivo exposure to cocaine abolishes endocannabinoid mGluR5-mediated retrograde long-term depression (LTD) and decreases the surface expression of mGluR5 in the mouse accumbens (Fourgeaud et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

“…In cell cultures and mice brain slices, mGluR1a and mGluR5 undergo agonist-stimulated internalization and endocytosis (Dale et al, 2001;Mundell et al, 2001) which, in some cases, was correlated with decreased group I mGluR-mediated physiological effects (Fourgeaud et al, 2004). However, there has been no in vivo study looking at changes in the trafficking of group I mGluRs following glutamate or receptor agonist stimulation in the mammalian brain.…”

Section: Introductionmentioning

confidence: 99%

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Subcellular and subsynaptic localization of group I metabotropic glutamate receptors in the nucleus accumbens of cocaine-treated rats

2008

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There is significant pharmacological and behavioral evidence that group I metabotropic glutamate receptors (mGluR1a and mGluR5) in the nucleus accumbens play an important role in the neurochemical and pathophysiological mechanisms that underlie addiction to psychostimulants. To further address this issue, we undertook a detailed ultrastructural analysis to characterize changes in the subcellular and subsynaptic localization of mGluR1a and mGluR5 in the core and shell of nucleus accumbens following acute or chronic cocaine administration in rats. After a single cocaine injection (30mg/kg) and 45 minutes withdrawal, there was a significant decrease in the proportion of plasma membrane-bound mGluR1a in accumbens shell dendrites. Similarly, the proportion of plasma membrane-bound mGluR1a was decreased in large dendrites of accumbens core neurons following chronic cocaine exposure (i.e. 1 week treatment followed by three weeks withdrawal). However, neither acute nor chronic cocaine treatments induced significant change in the localization of mGluR5 in accumbens core and shell, which is in contrast with the significant reduction of plasma membranebound mGluR1a and mGluR5 induced by local intra-accumbens administration of the group I mGluR agonist, DHPG. In conclusion, these findings demonstrate that cocaine-induced glutamate imbalance (Smith et al., 1995;Pierce et al., 1996;Reid et al., 1997) has modest effects on the trafficking of group I mGluRs in the nucleus accumbens. These results provide valuable information on the neuroadaptive mechanisms of accumbens group I mGluRs in response to cocaine administration.

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Comparative analysis of the subcellular and subsynaptic localization of mGluR1a and mGluR5 metabotropic glutamate receptors in the shell and core of the nucleus accumbens in rat and monkey

Mitrano

Smith

2006

J of Comparative Neurology

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Group I metabotropic glutamate receptors (mGluRs) play critical roles in synaptic plasticity and drug addiction. To characterize potential sites whereby these receptors mediate their effects in the ventral striatum, we studied the subcellular and subsynaptic localization of mGluR1a and mGluR5 in the shell and core of the nucleus accumbens in rat and monkey. In both species, group I mGluRs are mainly postsynaptic in dendrites and spines, with rare presynaptic labeling in unmyelinated axons. Minor, yet significant, differences in proportions of specific immunoreactive elements were found between the accumbens shell and the accumbens core in monkey. At the subsynaptic level, significant differences were found in the proportion of plasma membrane-bound mGluR5 labeling between species. In dendrites, spines, and unmyelinated axons, a significantly larger proportion of mGluR5 labeling was bound to the plasma membrane in rats (50-70%) than in monkeys (30-50%). Conversely, mGluR1a displayed the same pattern of immunogold labeling in the two species. Electron microscopic colocalization studies revealed 30% colocalization of mGluR1a and mGluR5 in dendrites and as much as 50-65% in spines in both compartments of the rat accumbens. Both group I mGluRs were significantly expressed in D1-immunoreactive dendritic processes (60-75% colocalization) and spines (30-50%) of striatal projection neurons as well as dendrites of cholinergic (30-70%) and parvalbumin-containing (70-85%) interneurons. These findings highlight the widespread expression of group I mGluRs in projection neurons and interneurons of the shell and core of the nucleus accumbens, providing a solid foundation for regulatory and therapeutic functions of group I mGluRs in reward-related behaviors and drug addiction.

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A SingleIn VivoExposure to Cocaine Abolishes Endocannabinoid-Mediated Long-Term Depression in the Nucleus Accumbens

Cited by 188 publications

References 39 publications

Acute Amphetamine Exposure Selectively Desensitizes κ-Opioid Receptors in the Nucleus Accumbens

Acute Amphetamine Exposure Selectively Desensitizes κ-Opioid Receptors in the Nucleus Accumbens

Subcellular and subsynaptic localization of group I metabotropic glutamate receptors in the nucleus accumbens of cocaine-treated rats

Comparative analysis of the subcellular and subsynaptic localization of mGluR1a and mGluR5 metabotropic glutamate receptors in the shell and core of the nucleus accumbens in rat and monkey

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