Extended Data Fig. 12: SOROXT affects aVMHvl cell activity by activating OXTR, not glutamatergic synaptic transmission.
From: A dedicated hypothalamic oxytocin circuit controls aversive social learning
a. Strategy to evaluate OXTR knockout efficiency. b. Representative recording traces of GFP cells from knockout (KO) and control (Ctrl) sides under TGOT perfusion (red bar). c. Number of aVMHvl cells (from 4 animals) depolarized ( > 4 mV) by TGOT in KO and control sides. Chi-square’s test. **p < 0.01. d. Representative traces showing the membrane potential changes of two aVMHvl cells, one recorded in ACSF (d1) and the other in the presence of 1 µM L-368, 889, a highly specific OXTR antagonist (d2). e. The number of cells depolarized (ΔRMP > 4 mV) by the SOROXT optogenetic stimulation (20 Hz, 1 ms, 5 min) and not. n = 23 (without OXTRA) cells from 5 animals and 23 (with OXTRA) cells from 4 animals. Chi-square’s test. ****p < 0.0001. f-h. Histology images showing oxytocin (OXT, red) immunostaining and Vglut2 (green) expression in the PVN (f), SON (g), and SOR (h) from Vglut2Cre:Ai6 male mice. Scale bars: 50 µm. i. The percentage of OXT-positive cells that express Vglut2 in the PVN, SON, and SOR. Circles represent individual animals. Plotted as mean±s.e.m. n = 3 male mice. j. Slice recording schematics. k-l. Representative voltage clamp recording traces from aVMHvlOXTR cells when a 1 ms light pulse (blue vertical bar) was delivered to activated PVNOXT (k) or SOROXT (l) input. m. None of the aVMHvlOXTR cells showed light-evoked EPSC during PVNOXT (0/14 cells) or SOROXT optogenetic activation (0/12 cells). See Supplementary Table 1 for detailed statistics.
