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Fig. 5 | Molecular Autism

Fig. 5

From: Imbalance of flight–freeze responses and their cellular correlates in the Nlgn3−/y rat model of autism

Fig. 5

Hyperexcitability of dorsal, but not ventral PAG neurons in Nlgn3−/y rats. A, E Schematics of PAG slice indicating area recorded from in grey. B dPAG cells from Nlgn3−/y rats fire increased numbers of action potentials in response to increasing current injection steps (p = 0.018, F(1, 17) = 6.87, repeated measures two-way ANOVA, WT n = 25 cells/ 10 rats, KO n = 26 cells/ 9 rats). Representative traces of rheobase and + 100 pA steps for WT (black) and Nlgn3−/y (purple) dPAG cells. C dPAG cells from Nlgn3−/y rats have lower rheobase potential than WT (p = 0.014, GLMM, WT n = 25 cells/ 10 rats, KO n = 26 cells/ 9 rats). D No change in mEPSC amplitude or frequency of dPAG neurons in Nlgn3−/y rats compared to WT (amplitude: p = 0.28, frequency p= 0.61, GLMM, WT 12 cells/ 6 rats, KO 13 cells/ 6 rats). Representative traces of mEPSCs of dPAG cells from WT (black) and Nlgn3−/y (purple) rats. F vPAG cells from Nlgn3−/y and WT rats fire comparable numbers of action potentials in response to increasing current injection steps (p = 0.54, F(1, 17) = 0.38, repeated measures two-way ANOVA, WT n = 24 cells/ 9 rats, KO n = 28 cells/ 10 rats). Representative traces of rheobase and + 100 pA steps for WT (black) and Nlgn3−/y (purple) vPAG cells. G vPAG cells from Nlgn3−/yrats have a comparable rheobase potential to WT cells (p = 0.4, GLMM, WT n = 24 cells/ 9 rats, KO 28 cells/ 10 rats). H No change in mEPSC amplitude or frequency of vPAG neurons in Nlgn3−/y rats in comparison to WT (amplitude: = 0.78, frequency: p = 0.88, GLMM, WT n=24 cells/ 9 rats KO n=28 cells/ 10 rats). Data represented as mean ± SEM, dots represent individual cells

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