Na<sub>v</sub>1.7 is the predominant sodium channel in rodent olfactory sensory neurons
<p>Abstract</p> <p>Background</p> <p>Voltage-gated sodium channel Na<sub>v</sub>1.7 is preferentially expressed in dorsal root ganglion (DRG) and sympathetic neurons within the peripheral nervous system. Homozygous or compound heterozygous loss-of-function m...
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2011-05-01T00:00:00Z.
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|---|---|---|---|
| 001 | doaj_bcab5dcf363a48f2bd3136fdda6769e0 | ||
| 042 | |a dc | ||
| 100 | 1 | 0 | |a Black Joel A |e author |
| 700 | 1 | 0 | |a Ahn Hye-Sook |e author |
| 700 | 1 | 0 | |a Zhao Peng |e author |
| 700 | 1 | 0 | |a Tyrrell Lynda |e author |
| 700 | 1 | 0 | |a Waxman Stephen G |e author |
| 700 | 1 | 0 | |a Dib-Hajj Sulayman D |e author |
| 245 | 0 | 0 | |a Na<sub>v</sub>1.7 is the predominant sodium channel in rodent olfactory sensory neurons |
| 260 | |b SAGE Publishing, |c 2011-05-01T00:00:00Z. | ||
| 500 | |a 10.1186/1744-8069-7-32 | ||
| 500 | |a 1744-8069 | ||
| 520 | |a <p>Abstract</p> <p>Background</p> <p>Voltage-gated sodium channel Na<sub>v</sub>1.7 is preferentially expressed in dorsal root ganglion (DRG) and sympathetic neurons within the peripheral nervous system. Homozygous or compound heterozygous loss-of-function mutations in <it>SCN9A</it>, the gene which encodes Na<sub>v</sub>1.7, cause congenital insensitivity to pain (CIP) accompanied by anosmia. Global knock-out of Na<sub>v</sub>1.7 in mice is neonatal lethal reportedly from starvation, suggesting anosmia. These findings led us to hypothesize that Na<sub>v</sub>1.7 is the main sodium channel in the peripheral olfactory sensory neurons (OSN, also known as olfactory receptor neurons).</p> <p>Methods</p> <p>We used multiplex PCR-restriction enzyme polymorphism, <it>in situ </it>hybridization and immunohistochemistry to determine the identity of sodium channels in rodent OSNs.</p> <p>Results</p> <p>We show here that Na<sub>v</sub>1.7 is the predominant sodium channel transcript, with low abundance of other sodium channel transcripts, in olfactory epithelium from rat and mouse. Our <it>in situ </it>hybridization data show that Na<sub>v</sub>1.7 transcripts are present in rat OSNs. Immunostaining of Na<sub>v</sub>1.7 and Na<sub>v</sub>1.6 channels in rat shows a complementary accumulation pattern with Na<sub>v</sub>1.7 in peripheral presynaptic OSN axons, and Na<sub>v</sub>1.6 primarily in postsynaptic cells and their dendrites in the glomeruli of the olfactory bulb within the central nervous system.</p> <p>Conclusions</p> <p>Our data show that Na<sub>v</sub>1.7 is the dominant sodium channel in rat and mouse OSN, and may explain anosmia in Na<sub>v</sub>1.7 null mouse and patients with Na<sub>v</sub>1.7-related CIP.</p> | ||
| 546 | |a EN | ||
| 690 | |a Pathology | ||
| 690 | |a RB1-214 | ||
| 655 | 7 | |a article |2 local | |
| 786 | 0 | |n Molecular Pain, Vol 7, Iss 1, p 32 (2011) | |
| 787 | 0 | |n http://www.molecularpain.com/content/7/1/32 | |
| 787 | 0 | |n https://doaj.org/toc/1744-8069 | |
| 856 | 4 | 1 | |u https://doaj.org/article/bcab5dcf363a48f2bd3136fdda6769e0 |z Connect to this object online. |