The Central Amygdala and Alcohol: Role of g-Aminobutyric Acid, Glutamate, and Neuropeptides

نویسندگان

  • Marisa Roberto
  • Nicholas W. Gilpin
  • George R. Siggins
چکیده

Alcohol dependence is a chronically relapsing disorder characterized by compulsive drug seeking and drug taking, loss of control in limiting intake, and the emergence of a withdrawal syndrome in the absence of the drug. Accumulating evidence suggests an important role for synaptic transmission in the central amygdala (CeA) in mediating alcohol-related behaviors and neuroadaptative mechanisms associated with alcohol dependence. Acute alcohol facilitates g-aminobutyric acid-ergic (GABAergic) transmission in CeA via both preand postsynaptic mechanisms, and chronic alcohol increases baseline GABAergic transmission. Acute alcohol inhibits glutamatergic transmission via effects at N-methyl-D-aspartate (NMDA) and AMPA receptors in CeA, whereas chronic alcohol up-regulates N-methylD-aspartate receptor (NMDAR)-mediated transmission. Pro(e.g., corticotropin-releasing factor [CRF]) and anti-stress (e.g., NPY, nociceptin) neuropeptides affect alcoholand anxiety-related behaviors, and also alter the alcohol-induced effects on CeA neurotransmission. Alcohol dependence produces plasticity in these neuropeptide systems, reflecting a recruitment of those systems during the transition to alcohol dependence.

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The central amygdala and alcohol: role of γ-aminobutyric acid, glutamate, and neuropeptides.

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تاریخ انتشار 2012