Full text is available at the source.
Abstract
Postnatal knockout of Creld1 in dorsal root ganglion neurons resulted in profound behavioral deficits in touch, temperature, pain, and itch.
- Somatosensation is mediated by dorsal root ganglion neurons that convert physical and chemical stimuli into electrical signals.
- A targeted screen of 20 genes in mice identified Creld1 as a cross-model regulator of somatosensation.
- Knockout of Creld1 significantly impaired the ability to sense touch, temperature, pain, and itch.
- Overexpression of Creld1 enhanced responses to touch and thermal stimuli.
- CRELD1 is suggested to act as an auxiliary regulator of voltage-gated sodium channels, influencing neuron excitability.
Simplified