Chemosensory representation of first-time oral exposure to ethanol in the orbitofrontal cortex of mice.

Intermittent ethanol consumption changes the neuronal activity of the orbitofrontal cortex (OFC) in rodents, which has been attributed to important participation in the development of addiction, particularly alcoholism. The OFC participates in gustatory sensory integration. However, it is unknown whether this region can encode chemosensory elements of oral ethanol administration independently of the consumption movement (orofacial motor response) when administered for the first time (naïve mice).

Sensory-motor response elicited by first time intraoral administered ethanol after trigeminal neuropathic injury.

Recent findings have shown a relationship between alcohol use disorders (AUD) and chronic pain. Preclinical models have demonstrated that chronic pain, including trigeminal nerve injury, increases ethanol consumption throughout extended administration periods. Nevertheless, it remains unclear whether chronic pain induces a greater susceptibility to developing AUD by altering motor control consumption regardless of the symptomatology of neuropathic pain, and whether sex influences this susceptibility.