Drug-Evoked Synaptic Plasticity Causing Addictive Behavior

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Drug-evoked synaptic plasticity causing addictive behavior.

Introduction The clinical manifestations of drug addiction are the subject of medical literature and fiction alike. In Novel with Cocaine, first published almost 80 years ago under a pseudonym and only recently rediscovered, Mark Levi provides a disturbing account of a young Russian man becoming addicted to cocaine. Vadim, the novel’s antihero reflects: “Before I came in contact with cocaine I ...

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As in other parts of the central nervous system (CNS) of the mouse, glutamatergic synapses onto dopamine (DA) neurons in the ventral tegmental area (VTA) mature postnatally. At birth many AMPA receptors (AMPARs) lack GluA2R subunit and most NMDARs contain the GluN2B subunit. Within 2 weeks these receptors are replaced with GluA2- and GluN2A- containing AMPARs and NMDARs, respectively. Recent da...

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Drug-evoked synaptic plasticity: beyond metaplasticity.

Addictive drugs such as cocaine induce synaptic plasticity in the ventral tegmental area and its projection areas, which may represent the cellular correlate of an addiction trace. Cocaine induces changes in excitatory transmission primarily in the VTA, which persists for days after a single exposure. These initial alterations in synaptic transmission represent a metaplasticity that is permissi...

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Dopamine Enables In Vivo Synaptic Plasticity Associated with the Addictive Drug Nicotine

Addictive drugs induce a dopamine signal that contributes to the initiation of addiction, and the dopamine signal influences drug-associated memories that perpetuate drug use. The addiction process shares many commonalities with the synaptic plasticity mechanisms normally attributed to learning and memory. Environmental stimuli repeatedly linked to addictive drugs become learned associations, a...

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Drug-Evoked Synaptic Plasticity in Addiction: From Molecular Changes to Circuit Remodeling

Addictive drugs have in common that they target the mesocorticolimbic dopamine (DA) system. This system originates in the ventral tegmental area (VTA) and projects mainly to the nucleus accumbens (NAc) and prefrontal cortex (PFC). Here, we review the effects that such drugs leave on glutamatergic and GABAergic synaptic transmission in these three brain areas. We refer to these changes as drug-e...

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ژورنال

عنوان ژورنال: Journal of Neuroscience

سال: 2013

ISSN: 0270-6474,1529-2401

DOI: 10.1523/jneurosci.3406-13.2013