Glutamate plasticity in the drunken amygdala: the making of an anxious synapse

Int Rev Neurobiol. 2010;91:205-33. doi: 10.1016/S0074-7742(10)91007-6.

Abstract

Plasticity at glutamatergic synapses is believed to be the cellular correlate of learning and memory. Classic fear conditioning, for example, is dependent upon NMDA-type glutamate receptor activation in the lateral/basolateral amygdala followed by increased synaptic expression of AMPA-type glutamate receptors. This review provides an extensive comparison between the initiation and expression of glutamatergic plasticity during learning/memory and glutamatergic alterations associated with chronic ethanol exposure and withdrawal. The parallels between these neuro-adaptive processes suggest that long-term ethanol exposure might "chemically condition" amygdala-dependent fear/anxiety via the increased function of pre- and post-synaptic glutamate signaling.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Alcoholism / pathology*
  • Amygdala* / drug effects
  • Amygdala* / pathology
  • Amygdala* / physiopathology
  • Animals
  • Ethanol / pharmacology*
  • Glutamic Acid / metabolism*
  • Humans
  • Neuronal Plasticity / drug effects*
  • Receptors, AMPA / metabolism
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Synapses / drug effects*
  • Synapses / physiology

Substances

  • Receptors, AMPA
  • Receptors, N-Methyl-D-Aspartate
  • Ethanol
  • Glutamic Acid