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Drug-Evoked Synaptic Plasticity in Addiction: From Molecular Changes to Circuit Remodeling
被引:805
作者:

Luescher, Christian
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h-index: 0
机构:
Univ Geneva, Dept Basic Neurosci, CH-1211 Geneva, Switzerland
Univ Geneva, Neurol Clin, CH-1211 Geneva, Switzerland Univ Geneva, Dept Basic Neurosci, CH-1211 Geneva, Switzerland

Malenka, Robert C.
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h-index: 0
机构:
Stanford Univ, Sch Med, Nancy Pritzker Lab, Dept Psychiat & Behav Sci, Palo Alto, CA 94305 USA Univ Geneva, Dept Basic Neurosci, CH-1211 Geneva, Switzerland
机构:
[1] Univ Geneva, Dept Basic Neurosci, CH-1211 Geneva, Switzerland
[2] Univ Geneva, Neurol Clin, CH-1211 Geneva, Switzerland
[3] Stanford Univ, Sch Med, Nancy Pritzker Lab, Dept Psychiat & Behav Sci, Palo Alto, CA 94305 USA
来源:
关键词:
VENTRAL TEGMENTAL AREA;
LONG-TERM DEPRESSION;
RECEPTOR SUBUNIT EXPRESSION;
MIDBRAIN DOPAMINE NEURONS;
EXCITATORY AMINO-ACIDS;
MEDIUM SPINY NEURONS;
IN-VIVO EXPOSURE;
NUCLEUS-ACCUMBENS;
BEHAVIORAL SENSITIZATION;
NMDA-RECEPTORS;
D O I:
10.1016/j.neuron.2011.01.017
中图分类号:
Q189 [神经科学];
学科分类号:
071006 ;
摘要:
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-evoked synaptic plasticity, which outlasts the presence of the drug in the brain and contributes to the reorganization of neural circuits. While in most cases these early changes are not sufficient to induce the disease, with repetitive drug exposure, they may add up and contribute to addictive behavior.
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页码:650 / 663
页数:14
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