Genetic inactivation of the CRF1 receptor eliminates morphine-induced sociability deficits and neuronal firing.
(A) Experimental procedure. Male CRF1+/+, CRF1+/− and CRF1−/− mice were injected intraperitoneally (i.p.) with either saline or morphine (0.625 mg/kg) and tested in the three-chamber task for sociability. Additional groups of male CRF1+/+, CRF1+/− and CRF1−/− mice were injected with either saline or morphine (0.625 mg/kg) and cell-attached patch-clamp recordings of paraventricular nucleus of the hypothalamus (PVN) neurons performed from brain slices. Time (s) spent in the regions of interest (ROIs, side half-chambers) of the three-chamber apparatus (see Fig. 1A) during the (B) habituation and the (C) sociability phase of the test, (D) sociability ratio (%) and (E) firing frequency (Hz) of PVN neurons by saline- or morphine-treated CRF1+/+, CRF1+/− and CRF1−/− mice. (F) Images showing electrophysiological recordings from PVN neurons of the six experimental groups. The number of animals and the number of patched and recorded cells within each experimental group is reported in Table S1B. Values represent mean±SEM. *P<0.05, **P<0.005, ***P<0.0005.