Bradley Kenneth Taylor

This study investigates the role of ATF3 in pain following tissue damage, finding that axonal injury is necessary and sufficient for ATF3 induction, while inflammation and action potential conduction are not required.

The paper identifies parabrachial neurons expressing the NPY Y1 receptor as a hub that suppresses sustained pain through NPY signaling.

The paper shows that MOR and Y1R receptor synergy in spinal cord interneurons reduces postoperative hyperalgesia and ongoing pain after surgery.

The paper identifies a parabrachial-to-amygdala circuit mediated by CGRP that drives hemispheric lateralization of visceral pain processing in mice.

The paper characterizes firing patterns of Y1eGFP neurons in the spinal cord and finds they exhibit delayed short-latency firing under hyperpolarized conditions, associated with fast A-type potassium currents and T-type calcium channel activity.