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. Author manuscript; available in PMC: 2021 Mar 15.
Published in final edited form as: Neuropharmacology. 2019 Dec 21;165:107831. doi: 10.1016/j.neuropharm.2019.107831

Figure 3. KOR activation increased glutamate release and reduced GABA release on SN-projecting IC neurons.

Figure 3.

(A) IC-SN neurons were labeled for whole-cell recordings using fluorescent retrobeads injected into the SN. (B) Compared to baseline (BL), 10 min bath application of dynorphin A (Dyn, 300 nM) significantly increased spontaneous excitatory postsynaptic current (sEPSC) frequency but not amplitude, *p < 0.05 and (C) reduced spontaneous inhibitory postsynaptic current (sIPSC) frequency but not amplitude in IC-SN cells, **p < 0.01. (D) Dyn increased sEPSC/sIPSC (E/I) ratio in a sex-dependent manner; sex × drug interaction, #p < 0.01; significant increase in E/I in male mice, **p < 0.01. (E) Representative traces of sEPSCs (top) and sIPSCs (bottom) at baseline (black) and following Dyn (blue) wash-on. (F) The increase in sEPSC frequency, (G) decrease in sIPSC frequency, and (H) increase in E/I ratio by Dyn were blocked by pre-application of the KOR antagonist nor-BNI (100 nM), and sEPSC and sIPSC amplitude was not impacted. (I) Representative traces of sEPSCs and sIPSCs at baseline (black) and following Dyn (blue) wash-on in slices pretreated with nor-BNI. Females, open circles; males closed circles; n = 3 mice/sex (normal aCSF), n = 3 mice/sex (nor-BNI); BL, baseline; Dyn, dynorphin A