Heather N. Allen

This study demonstrates that vertical climbing in mice is a reliable and translationally relevant measure of pain-related functional impairment across multiple pain models.

This study investigates the effects of modulating the CRMP2-Nav1.7 interaction on trigeminal neuropathic pain, showing behavioral improvement without normalizing central pain circuit activity.

This study identifies NaV1.7-dependent peripheral sensitization as a mechanism of chronic pain in Parkinson's disease and highlights CRMP2 regulation of NaV1.7 as a therapeutic target.

This study shows that transient myotonia can cause long-lasting pain by altering nociceptive processing and identifies NaV1.8 as a target for analgesics.

This study shows that NRP1 in CGRP afferents is required for VEGFA-driven pain and baseline nociception in mice.

This study investigates the role of CeA CGRP in neuropathic pain, finding that it modulates cold sensitivity differently based on injury type and hemisphere.

The paper introduces a synthetic potassium channel that senses and mitigates oxidative stress by modulating membrane potential in cells and organelles.

This study identifies Brs3-expressing neurons in the parabrachial nucleus as a key population involved in heat hypersensitivity during persistent pain.

This study shows that CBD3063, a CRMP2 modulator, reduces OA pain in rodents by decreasing CaV2.2 membrane expression and neural activity.

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

The paper develops a CRMP2-Ubc9 inhibitor that reduces NaV1.7 activity and alleviates trigeminal neuropathic pain in rats.

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.