Target-Specific Suppression of GABA Release from Parvalbumin Interneurons in the Basolateral Amygdala by Dopamine

• DOI: 10.1523/jneurosci.2997-12.2012
• Publication Date: 2012-10-18T05:22:33Z
• Authors: Hong-Yuan Chu; Wataru Ito; Jiayang Li; Alexei Morozov
• Keywords: Male; 0301 basic medicine; Dopamine; Mice, Transgenic; Amygdala; GABA Antagonists; Mice, Inbred C57BL; Mice; 03 medical and health sciences; Parvalbumins; Inhibitory Postsynaptic Potentials; Interneurons; Animals; gamma-Aminobutyric Acid

Dopamine (DA) in the basolateral amygdala (BLA) promotes fear learning by disinhibiting principal neurons (PNs) and enabling synaptic plasticity in their sensory inputs. While BLA interneurons (INs) are heterogeneous, it is unclear which interneuron subtypes decrease GABAergic input to PNs in the presence of DA. Here, using cell type-selective photostimulation by channelrhodopsin 2 in BLA slices from mouse brain, we examined the role of parvalbumin-positive INs (PV-INs), the major interneuronal subpopulation in BLA, in the disinhibitory effect of DA. We found that DA selectively suppressed GABAergic transmission from PV-INs to PNs by acting on presynaptic D2receptors, and this effect was mimicked by Rp-cAMP, an inhibitor of cAMP-dependent signaling. In contrast, DA did not alter GABA release from PV-INs to INs. Furthermore, neither suppressing cAMP-dependent signaling by Rp-cAMP nor enhancing it by forskolin altered GABA release from PV-INs to BLA INs. Overall, DA disinhibits BLA, at least in part, by suppressing GABA release from PV-INs in the target cell-specific manner that results from differential control of this release by cAMP-dependent signaling.