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Publication : Selective gating of glutamatergic inputs to excitatory neurons of amygdala by presynaptic GABAb receptor.

First Author  Pan BX Year  2009
Journal  Neuron Volume  61
Issue  6 Pages  917-29
PubMed ID  19324000 Mgi Jnum  J:157367
Mgi Id  MGI:4430706 Doi  10.1016/j.neuron.2009.01.029
Citation  Pan BX, et al. (2009) Selective gating of glutamatergic inputs to excitatory neurons of amygdala by presynaptic GABAb receptor. Neuron 61(6):917-29
abstractText  GABAb receptor (GABAbR)-mediated suppression of glutamate release is critical for limiting glutamatergic transmission across the central nervous system (CNS). Here we show that, upon tetanic stimulation of afferents to lateral amygdala, presynaptic GABAbR-mediated inhibition only occurs in glutamatergic inputs to principle neurons (PNs), not to interneurons (INs), despite the presence of GABAbR in terminals to both types of neurons. The selectivity is caused by differential local GABA accumulation; it requires GABA reuptake and parallels distinct spatial distributions of presynaptic GABAbR in terminals to PNs and INs. Moreover, GABAbR-mediated suppression of theta-burst-induced long-term potentiation (LTP) occurs only in the inputs to PNs, not to INs. Thus, target-cell-specific control of glutamate release by presynaptic GABAbR orchestrates the inhibitory dominance inside amygdala and might contribute to prevention of nonadaptive defensive behaviors.
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