Selective gating of glutamatergic inputs to excitatory neurons of amygdala by presynaptic GABAb receptor.
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.
Pan
Bing-Xing
BX
Unit on Behavioral Genetics, Laboratory of Molecular Pathophysiology, National Institute of Mental Health, National Institutes of Health, 35 Convent Drive, Bethesda, MD 20892, USA. panb@mail.nih.gov
Dong
Yulin
Y
Ito
Wataru
W
Yanagawa
Yuchio
Y
Shigemoto
Ryuichi
R
Morozov
Alexei
A