Glutamate plasticity in the drunken amygdala: the making of an anxious synapse.
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.
McCool
Brian A
BA
Department of Physiology & Pharmcology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Christian
Daniel T
DT
Diaz
Marvin R
MR
Läck
Anna K
AK
D000437:Alcoholism / Q000473:pathology*; D000679:Amygdala / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D000818:Animals; D000431:Ethanol / Q000494:pharmacology*; D018698:Glutamic Acid / Q000378:metabolism*; D006801:Humans; D009473:Neuronal Plasticity / Q000187:drug effects*; D018091:Receptors, AMPA / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D013569:Synapses / Q000187:drug effects* / Q000502:physiology
D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate; D000431:Ethanol; D018698:Glutamic Acid
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