Article Figures & Data
Figures
- Figure 1.
Selective activation of GABAergic transmission between PV-INs and PNs in BLA by ChR2. A, Confocal images show ChR2-tdTomato fluorescence (red) and PV-immunofluorescence (blue). Note that all ChR2-expressing cells (arrows) express PV, but only 41 ± 4% of PV-INs (n = 4 mice) express ChR2. B, Left, Whole-cell recording from a ChR2-expressing neuron. Short pulses of photostimulation (Photo-stim) evoke membrane depolarization (red, 0.2 ms pulse) and action potential (black, 0.4 ms pulse). Right, Trains of action potentials induced by continuous photostimulation (red, firing frequency = 107 Hz) or by current injection (black, firing frequency = 70 Hz). C, Blockade of light-induced IPSCs by GABAA receptor antagonist picrotoxin. D, Blockade of light-induced IPSCs by P/Q type Ca2+ channel blocker ω-agatoxin IVA. Left, IPSCs examples before (black) and after (red) ω-agatoxin IVA application. Right, Summary bar graph shows the blockade of light-induced IPSCs by ω-agatoxin IVA (*p < 0.05). E, Lack of DSI in light-induced IPSCs by a 6 s depolarization to 0 mV.
- Figure 2.
Selective modulation of GABAergic transmission from PV-INs to PNs by DA. A, Expression of ChR2 (left) in BLA of Cre-PV/GAD67-GFP mice (middle). B, Recording configuration. C, Top, example IPSCs evoked in a BLA pyramidal neuron by photostimulation (Photo-stim) before (black) and after (red) DA application. Bottom, Time course of the IPSC amplitude in the same cell. D, Top, Example IPSCs evoked in a BLA INs by photostimulation before (black) and after (red) DA application. Bottom, Time course of the IPSCs amplitude in the same cell. E, Summarized data for the effects of DA in BLA PNs and INs. F, DA effect on GABAergic neurotransmission from SOM-INs to PNs and INs. The red and blue traces indicate IPSCs after DA application. **p < 0.01 when compared with baseline.
- Figure 3.
Presynaptic D2 receptor mediates the inhibitory effects of DA in PV-IN projections to PNs. A, Top, Example traces of synaptic responses to paired-pulse stimulation before (black) and after (red) DA application. Bottom, Summary graph shows changes of paired-pulse ratio during DA application. B, Top, Example traces of muscimol-puffing-induced GABAA receptor current before (black) and after (red) DA application. Bottom, Summary graph shows muscimol-induced current during DA application. C, Top, Firing pattern of a PV-IN expressing ChR2 upon photostimulation (light) before and after DA application. Bottom, Effects of DA on membrane potential (MP; left), input resistance (Rin; middle), and number of spikes (right) in PV-INs. D, Top, Example IPSC traces before and after DA application in the presence of raclopride (Rac), and the IPSC traces before and after application of quinpirole. Bottom, Summary bar graph shows inhibition of IPSC by DA, lack of such inhibition in the presence of raclopride, and inhibition by quinpirole. Each dot represents a single cell. **p < 0.01, ***p < 0.005. n.s., Nonsignificant, when compared with baseline.
- Figure 4.
The role of cAMP-dependent signaling in target-specific inhibition of GABA release from PV-INs by DA. A, Specific GIRK channel inhibitor tertiapin-Q did not interfere with DA inhibition of IPSCs in PNs. Left, Time course of IPSC amplitude from an example cell. Right, Summary graph showing the effect of DA after blockade of GIRK. Each symbol represents a single neuron. B, C, Inhibitory effect of DA was blocked by cAMP competitor Rp-cAMP (B) and by PKA inhibitor H-89 (C). D, E, Rp-cAMP alone reduced the IPSC amplitude in PNs (D) but not in INs (E). F, Adenylate cyclase activator forskolin did not affect GABA release from PV-INs to INs. *p < 0.05, **p < 0.01.
