Queensta Millet

The paper profiles transcriptomic and proteomic data from NaV1.8-expressing mouse nociceptors, identifying 353 transcripts and 78 proteins, and finds moderate correlation between proteome and transcriptome datasets.

This study identifies opioid-dependent inhibition of neurotransmitter release as the primary mechanism of analgesia in NaV1.7 null mutants in mice and humans.

The paper identifies silent cold-sensing neurons that become active in neuropathic pain and contribute to cold allodynia through peripheral sensitization.

This study shows that Nav1.7 from sensory neurons affects dorsal horn neuron excitability, with functional effects not predicted by mRNA levels.

The paper shows that Nav1.7 loss of function analgesia requires both mu and delta opioid receptors, and enkephalin upregulation alone is insufficient for analgesia.

The paper identifies 267 NaV1.7-associated proteins in mice using epitope-tagged gene targeting and mass spectrometry, including novel interactors validated by co-immunoprecipitation and functional assays.

This study shows that BDNF from peripheral sensory neurons is critical for transitioning acute to chronic pain.

This study identifies Annexin A6 as a modulator of somatosensory mechanotransduction by affecting mechanically-activated currents in sensory neurons.