Fig. 6: Chemogenetic inhibition of nNOS-expressing neurons suppressed CFA-induced AMPAR trafficking in the vmPFC. | Nature Communications

Fig. 6: Chemogenetic inhibition of nNOS-expressing neurons suppressed CFA-induced AMPAR trafficking in the vmPFC.

From: nNOS-expressing neurons in the vmPFC transform pPVT-derived chronic pain signals into anxiety behaviors

Fig. 6

a Experimental design for (b–f). Ten microliters of CFA or NS was injected into the hind paw, and AAV-hSyn-DIO-hM4Di-eGFP (0.2 μl) and AAV-CaMKIIα-mCherry (0.2 μl) were microinjected into the vmPFC of nNOS-Cre mice on the indicated day. b Representative traces of mEPSCs in layer 2/3 pyramidal neurons of the vmPFC 3 weeks after AAV injection into nNOS-Cre mice. c, d Cumulative fraction plots of mEPSC amplitude (c, mean amplitude in inset) and interevent intervals (d, mean frequency in inset). n = 14 neurons (from 6 mice). e Representative traces of eEPSCs in the presence of BMI in layer 2/3 pyramidal neurons of the vmPFC 3 weeks after AAV injection into nNOS-Cre mice. Arrows indicate that AMPAR-EPSCs were measured at their peak at a holding potential of −70 mV, and NMDAR-EPSCs were measured 50 ms after stimulation at a holding potential of +40 mV. f Dot plot showing the AMPA/NMDA ratio from (e). n = 10 neurons (from 4 mice). Data are the mean ± SEM; **p < 0.01, and ***p < 0.001. (one-way ANOVA followed by Tukey’s post hoc test). Source data are provided as a Source data file. Exact p values and additional statistical information can be found in Source data.

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