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. Author manuscript; available in PMC: 2021 Oct 28.
Published in final edited form as: Neuron. 2020 Sep 1;108(2):349–366.e6. doi: 10.1016/j.neuron.2020.07.039

Figure 2. CCK induced rNSC depolarization is mediated by a glutamatergic relay.

Figure 2.

(A-C) Sample changes in rNSCs Vm to 300 nM CCK8 peptide in the presence of (A) 100 μM APV, 10 μM NBQX, 100 μM AIDA, 50 μM bicuculline, and 1 μM TTX, (B) in ACSF, or (C) in 1 μM YM022.

(D) Comparison of peptide induced depolarization of rNSCs. p=(0.003,0.003) for (7,7,7) cells in (6, 4, 5) animals by Wilcoxon-Mann-Whitney test. Bars indicate mean ± SEM for rNSCs that depolarized >10 mV from baseline (circles). ANBAT = APV, NBQX, bicuculline, AIDA, TTX.

(E) Percent of rNSCs in (D) that responded >10 mV to CCK8 application.

(F-H) Sample recordings of rNSC Vm to chemogenetic activation of CCK interneurons during (F) GABAAR blockade, (G) combined blockade of GABAARs, iGluRs and mGluRs, and (H) when only GABAARs and iGluRs were blocked or when only GABAAR and mGluRs were blocked. Curve fits to data in red, yellow diamonds indicate delay time to Vm deflection.

(I) Comparison of depolarization magnitude during CNO application under indicated conditions. One-way ANOVA showed an effect by condition F(4,41)=10.18, p=8.1*10−6, and a post hoc Dunnett analysis gave individual p-values vs ACSF of (0.95,0.018,0.002,0.0008) for (9,11,9,10,7) cells from (6,10,8,7,5) animals. Bars indicate mean ± SEM for rNSCs that depolarized >10 mV (circles).

(J) Percent of rNSCs in (I) that depolarized >10 mV.

(K) Times from CNO application to initiation of depolarizing event. Bars indicate mean ± SEM. One-way ANOVA showed no effect of condition; F(3,23)=1.66, p=0.2 for (6,10,5,5) responding cells from (5,9,4,4) animals. See also Figure S2.