Relapse to maladaptive eating habits during dieting is often provoked by stress. 
Recently, we identified a role of dorsal medial prefrontal cortex (mPFC) neurons 
in stress-induced reinstatement of palatable food seeking in male rats. It is 
unknown whether endogenous neural activity in dorsal mPFC drives stress-induced 
reinstatement in female rats. Here, we used an optogenetic approach, in which 
female rats received bilateral dorsal mPFC microinjections of viral constructs 
coding light-sensitive eNpHR3.0-eYFP or control eYFP protein and intracranial 
fiber optic implants. Rats were food restricted and trained to lever press for 
palatable food pellets. Subsequently, pellets were removed, and lever pressing 
was extinguished; then the effect of bilateral dorsal mPFC light delivery on 
reinstatement of food seeking was assessed after injections of the 
pharmacological stressor yohimbine (an α-2 andrenoceptor antagonist) or pellet 
priming, a manipulation known to provoke food seeking in hungry rats. Dorsal 
mPFC light delivery attenuated yohimbine-induced reinstatement of food seeking 
in eNpHR3.0-injected but not eYFP-injected rats. This optical manipulation had 
no effect on pellet-priming-induced reinstatement or ongoing food-reinforced 
responding. Dorsal mPFC light delivery attenuated yohimbine-induced Fos 
immunoreactivity and disrupted neural activity during in vivo 
electrophysiological recording in awake rats. Optical stimulation caused 
significant outward currents and blocked electrically evoked action potentials 
in eNpHR3.0-injected but not eYFP-injected mPFC hemispheres. Light delivery 
alone caused no significant inflammatory response in mPFC. These findings 
indicate that intracranial light delivery in eNpHR3.0 rats disrupts endogenous 
dorsal mPFC neural activity that plays a role in stress-induced relapse to food 
seeking in female rats.