A common mechanism mediates long-term changes in synaptic transmission after chronic cocaine and morphine

Antonello Bonci; John T. Williams

doi:10.1016/S0896-6273(00)80082-3

A common mechanism mediates long-term changes in synaptic transmission after chronic cocaine and morphine

Antonello Bonci, John T. Williams

Vollum Institute

Research output: Contribution to journal › Article › peer-review

198 Scopus citations

Abstract

The mesolimbic system is known to play a role in self-administration of opioids and psychostimulants. Although morphine and cocaine act by separate cellular mechanisms initially, the present study describes a common change in synaptic regulation of dopamine cells in the ventral tegmental area 1 week after termination of chronic treatment with either drug. Normally, D1 receptor activation augmented the amplitude of a γ-aminobutyric acid type B (GABA(B)) inhibitory postsynaptic potential (IPSP), but in drug-experienced animals, D1 receptor activation caused an inhibition of the GABA(B) IPSP. The inhibition was blocked by adenosine A1 receptor antagonists and by agents that disrupted the metabolism of cAMP. This long-lasting dopamine-adenosine interaction may be one mechanism involved in dopamine-mediated craving and relapse to drug-seeking behaviors.

Original language	English (US)
Pages (from-to)	631-639
Number of pages	9
Journal	Neuron
Volume	16
Issue number	3
DOIs	https://doi.org/10.1016/S0896-6273(00)80082-3
State	Published - Mar 1996

ASJC Scopus subject areas

General Neuroscience

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10.1016/S0896-6273(00)80082-3

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title = "A common mechanism mediates long-term changes in synaptic transmission after chronic cocaine and morphine",

abstract = "The mesolimbic system is known to play a role in self-administration of opioids and psychostimulants. Although morphine and cocaine act by separate cellular mechanisms initially, the present study describes a common change in synaptic regulation of dopamine cells in the ventral tegmental area 1 week after termination of chronic treatment with either drug. Normally, D1 receptor activation augmented the amplitude of a γ-aminobutyric acid type B (GABA(B)) inhibitory postsynaptic potential (IPSP), but in drug-experienced animals, D1 receptor activation caused an inhibition of the GABA(B) IPSP. The inhibition was blocked by adenosine A1 receptor antagonists and by agents that disrupted the metabolism of cAMP. This long-lasting dopamine-adenosine interaction may be one mechanism involved in dopamine-mediated craving and relapse to drug-seeking behaviors.",

author = "Antonello Bonci and Williams, {John T.}",

note = "Funding Information: We thank Drs. T. V. Dunwiddie, N.R. Zahniser, P. Osborne, and G. L. Westbrook for helpful discussions on the work and manuscript. This work was supported by grants from the National Institutes of Health (DA04523 and DA08163) and the Markey Foundation. ",

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AU - Williams, John T.

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N2 - The mesolimbic system is known to play a role in self-administration of opioids and psychostimulants. Although morphine and cocaine act by separate cellular mechanisms initially, the present study describes a common change in synaptic regulation of dopamine cells in the ventral tegmental area 1 week after termination of chronic treatment with either drug. Normally, D1 receptor activation augmented the amplitude of a γ-aminobutyric acid type B (GABA(B)) inhibitory postsynaptic potential (IPSP), but in drug-experienced animals, D1 receptor activation caused an inhibition of the GABA(B) IPSP. The inhibition was blocked by adenosine A1 receptor antagonists and by agents that disrupted the metabolism of cAMP. This long-lasting dopamine-adenosine interaction may be one mechanism involved in dopamine-mediated craving and relapse to drug-seeking behaviors.

AB - The mesolimbic system is known to play a role in self-administration of opioids and psychostimulants. Although morphine and cocaine act by separate cellular mechanisms initially, the present study describes a common change in synaptic regulation of dopamine cells in the ventral tegmental area 1 week after termination of chronic treatment with either drug. Normally, D1 receptor activation augmented the amplitude of a γ-aminobutyric acid type B (GABA(B)) inhibitory postsynaptic potential (IPSP), but in drug-experienced animals, D1 receptor activation caused an inhibition of the GABA(B) IPSP. The inhibition was blocked by adenosine A1 receptor antagonists and by agents that disrupted the metabolism of cAMP. This long-lasting dopamine-adenosine interaction may be one mechanism involved in dopamine-mediated craving and relapse to drug-seeking behaviors.

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A common mechanism mediates long-term changes in synaptic transmission after chronic cocaine and morphine

Abstract

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