Aida Calderón‐Rivera

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.

Enabling wider access to human molecular neuroscience research in pain: A simple preservation method for human dorsal root ganglion neurons in Hibernate A media

This paper introduces a method to preserve human dorsal root ganglion neurons using Hibernate media, enabling easier access and transport for research.

Mechanism, and treatment of anti-CV2/CRMP5 autoimmune pain

This study investigates how anti-CV2/CRMP5 autoantibodies cause pain in paraneoplastic neurological syndromes and identifies potential treatments.

Neuropilin-1 is a co-receptor for NGF and TrkA-evoked pain

This paper identifies NRP1 as a co-receptor for NGF and TrkA pain signaling and shows that targeting NRP1 or GIPC1 can reduce chronic pain without opioid use.

Intranasal CRMP2-Ubc9 Inhibitor Regulates NaV1.7 to Alleviate Trigeminal Neuropathic Pain

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

Identification and targeting of a unique NaV1.7 domain driving chronic pain

The paper identifies a unique NaV1.7 domain that can be targeted to produce analgesia by disrupting its interaction with CRMP2.