Loss-of-function mutations in the pore-forming α subunit of the voltage-gated sodium channel 1.7 (Nav1.7) cause congenital indifference to pain and anosmia. We used immunohistochemical techniques to study Nav1.7 localization in the rat olfactory system in order to better understand its role in olfaction. We confirm that Nav1.7 is expressed on olfactory sensory axons and report its presence on vomeronasal axons, indicating an important role for Nav1.7 in transmission of pheromonal cues. Following neuroepithelial injury, Nav1.7 was transiently expressed by cells of monocytic lineage. These findings support an emerging role for Nav1.7 in immune function. This sodium channel may provide an important pharmacological target for treatment of infla...
Expression of the voltage-gated sodium channel NaV1.7 in sensory neurons is required for pain sensat...
Chronic pain often represents a severe, debilitating condition. Up to 10% of the worldwide populatio...
We used a mouse with deletion of exons 4, 5, and 6 of the SCN11A (sodium channel, voltage-gated, typ...
Loss-of-function mutations in the pore-forming alpha subunit of the voltage-gated sodium channel 1.7...
Loss-of-function mutations in the pore-forming alpha subunit of the voltage-gated sodium channel 1.7...
Abstract Background Voltage-gated sodium channel Nav1.7 is preferentially expressed in dorsal root g...
Two voltage gated sodium channels, Nav1.8 and Nav1.9, are exclusively expressed in primary sensory n...
Chronic pain is a highly unmet clinical need; often treatment is only partially effective, and is fr...
Human voltage-activated sodium (Nav) channels are adept at rapidly transmitting electrical signals a...
Human voltage-activated sodium (Nav) channels are adept at rapidly transmitting electrical signals a...
The voltage-gated sodium channel NaV1.7 plays a critical role in pain pathways. We generated an epit...
Nav1.7, a peripheral neuron voltage-gated sodium channel, is essential for pain and olfaction in mic...
International audienceThe voltage-gated sodium channel Na V 1.7 plays a critical role in pain pathwa...
SummaryNav1.7, a peripheral neuron voltage-gated sodium channel, is essential for pain and olfaction...
Recent scientific discoveries have confirmed a pivotal role for the NaV 1.7 voltage-gated sodium cha...
Expression of the voltage-gated sodium channel NaV1.7 in sensory neurons is required for pain sensat...
Chronic pain often represents a severe, debilitating condition. Up to 10% of the worldwide populatio...
We used a mouse with deletion of exons 4, 5, and 6 of the SCN11A (sodium channel, voltage-gated, typ...
Loss-of-function mutations in the pore-forming alpha subunit of the voltage-gated sodium channel 1.7...
Loss-of-function mutations in the pore-forming alpha subunit of the voltage-gated sodium channel 1.7...
Abstract Background Voltage-gated sodium channel Nav1.7 is preferentially expressed in dorsal root g...
Two voltage gated sodium channels, Nav1.8 and Nav1.9, are exclusively expressed in primary sensory n...
Chronic pain is a highly unmet clinical need; often treatment is only partially effective, and is fr...
Human voltage-activated sodium (Nav) channels are adept at rapidly transmitting electrical signals a...
Human voltage-activated sodium (Nav) channels are adept at rapidly transmitting electrical signals a...
The voltage-gated sodium channel NaV1.7 plays a critical role in pain pathways. We generated an epit...
Nav1.7, a peripheral neuron voltage-gated sodium channel, is essential for pain and olfaction in mic...
International audienceThe voltage-gated sodium channel Na V 1.7 plays a critical role in pain pathwa...
SummaryNav1.7, a peripheral neuron voltage-gated sodium channel, is essential for pain and olfaction...
Recent scientific discoveries have confirmed a pivotal role for the NaV 1.7 voltage-gated sodium cha...
Expression of the voltage-gated sodium channel NaV1.7 in sensory neurons is required for pain sensat...
Chronic pain often represents a severe, debilitating condition. Up to 10% of the worldwide populatio...
We used a mouse with deletion of exons 4, 5, and 6 of the SCN11A (sodium channel, voltage-gated, typ...