Fig. 6.

Role of α6*-nAChRs and atypical GABA receptors in CIN inhibitory plasticity. A Illustration showing the experimental framework, wherein Cre-dependent AAV-DIO-ChR2-mCherry was injected into the VTA in VGAT-Cre/GAD67-GFP mice and optically evoked IPSCs were recorded in NAc CINs in whole-cell, voltage-clamp mode. Activation of GABAergic inputs to NAc CINs from the VTA were obtained by blue light stimulation through the objective. B Inset shows representative oIPSCs evoked in NAc CINs before and after low frequency optical stimulation (LFS; 1 Hz, 240 pulses). LFS reduced GABAergic oIPSCs in NAc CINs, termed CIN-iLTD. Horizontal markers pre (green) and post (red) indicate times where comparisons between treatment conditions were performed. C Superfusion of MII or treatment with α6-miRNA reduced CIN-iLTD. D Superfusion of the GABA receptor ρ−1 antagonist TPMPA markedly reduced CIN-iLTD. E Chronic exposure to EtOH reduced CIN-iLTD and produced a mild LTP state. F Summary of drug and treatment effects on CIN-iLTD. Values in parentheses are n values. Asterisks ** and *** indicate significance levels p < 0.01 and p < 0.001, respectively, for comparisons to baseline. Hashtags #, ##, and ### represent significance levels p < 0.05, p < 0.01, and p < 0.001, respectively, for comparisons between control and treatment responses