Tyler S. Nelson

A mouse model of myotonic dystrophy type 1 exhibits pain-like behavior and peripheral nociceptor hyperexcitability

This study identifies peripheral nociceptor hyperexcitability as a mechanism underlying pain in DM1 using a mouse model.

NaV1.7-dependent peripheral sensitization drives chronic pain in Parkinson's disease

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.

Myotonic Muscle Activity Drives a Persistent Pain State Responsive to NaV1.8-directed Analgesics

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

Neuropilin-1 in CGRP Afferents Is Required for VEGFA-Driven Pain and Baseline Nociceptive Sensitivity

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

Amygdalar Calcitonin Gene-Related Peptide Driven Effects of Cold Sensitivity Induced by Peripheral Neuropathy 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.

A synthetic potassium channel reduces oxidative stress 1 via cellular adaptronics

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

Parabrachial bombesin receptor subtype 3 neurons facilitate heat hypersensitivity in persistent pain

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

Uncoupling the CRMP2-CaV2.2 interaction reduces pain-like behavior in a preclinical osteoarthritis model

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

Parabrachial Calca neurons drive nociplasticity

This study shows that activation of parabrachial Calca neurons is necessary for chronic pain after nerve ligation and sufficient to drive nociplasticity in mice.

A parabrachial hub for the prioritization of survival behavior

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

Endogenous μ-opioid - neuropeptide Y Y1 receptor synergy silences chronic postoperative pain

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