Fig. 2: Neuropathic pain increases mPFC CRF neuronal activity, contributing to morphine reward facilitation. | Translational Psychiatry

Fig. 2: Neuropathic pain increases mPFC CRF neuronal activity, contributing to morphine reward facilitation.

From: A medial prefrontal cortex-nucleus acumens corticotropin-releasing factor circuitry for neuropathic pain-increased susceptibility to opioid reward

Fig. 2

a Typical images of mPFC CRF neurons. CRF-Cre mice were crossed with Ai9 mice to produce transgenic mice with red tdTomato-expressing neurons (a1). The tdTomato signal was completely colocalized with the CRF (a2, green), based on immunofluorescence staining (a3 and a4, yellow). Scale bars=200 μm for a1, a2, and a3; 50 μm for a4. b and c The threshold (b) and number (c) of action potentials evoked by depolarizing current pulses of various amplitudes in CCI and sham mice (n = 15–22 neurons). d Schematic of mPFC infusion of Cre-dependent AAV-hM4Di and intraperitoneal (i.p.) injection of CNO in CRF-Cre mice (left). The right picture is the typical image of injection sites and viral expression within the mPFC. e A representative trace (top) from a whole-cell current-clamp electrophysiological recording showing that bath application of CNO hyperpolarized glutamatergic neurons in the mPFC and statistics (bottom) showing the average magnitude of hyperpolarization (n = 6 neurons). f Behavioral effects caused by mPFC injection of hM4Di-mCherry in CRF-Cre mice with CCI (0.3 mg/kg morphine) or sham (1 mg/kg morphine) surgery after i.p. injection of saline or CNO (n = 6–8 mice). The data are expressed as the mean ± SEM. *p < 0.05; **p < 0.01

Back to article page