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Keywords
(15)
Central Nervous System
Immunohistochemi...
Multiplex Pcr
Olfactory Bulb
Olfactory Epithelium
Olfactory Receptor Neuron
Olfactory Sensory Neuron
Peripheral Nervous System
Polymorphism
Sodium Channel
Sympathetic Neuron
voltage-gated sodium channel
Dorsal Root Ganglion
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Restriction Enzyme
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Na v 1.7 is the predominant sodium channel in rodent olfactory sensory neurons
Na v 1.7 is the predominant sodium channel in rodent olfactory sensory neurons,10.1186/1744-8069-7-32,Molecular Pain,Hye-Sook Ahn,Joel A Black,Peng Zh
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Na v 1.7 is the predominant sodium channel in rodent olfactory sensory neurons
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Hye-Sook Ahn
,
Joel A Black
,
Peng Zhao
,
Lynda Tyrrell
,
Stephen G Waxman
,
Sulayman D Dib-Hajj
Background Voltage-gated
sodium channel
Nav1.7 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 SCN9A, the gene which encodes Nav1.7, cause congenital insensitivity to pain (CIP) accompanied by anosmia. Global knock-out of Nav1.7 in mice is neonatal lethal reportedly from starvation, suggesting anosmia. These findings led us to hypothesize that Nav1.7 is the main
sodium channel
in the peripheral olfactory sensory neurons (OSN, also known as
olfactory receptor
neurons). Methods We used multiplex PCR-restriction
enzyme
polymorphism, in situ hybridization and
immunohistochemistry
to determine the identity of sodium channels in rodent OSNs. Results We show here that Nav1.7 is the predominant
sodium channel
transcript, with low abundance of other
sodium channel
transcripts, in
olfactory epithelium
from rat and mouse. Our in situ hybridization data show that Nav1.7 transcripts are present in rat OSNs. Immunostaining of Nav1.7 and Nav1.6 channels in rat shows a complementary accumulation pattern with Nav1.7 in peripheral presynaptic OSN axons, and Nav1.6 primarily in postsynaptic cells and their dendrites in the glomeruli of the
olfactory bulb
within the central nervous system. Conclusions Our data show that Nav1.7 is the dominant
sodium channel
in rat and mouse OSN, and may explain anosmia in Nav1.7 null mouse and patients with Nav1.7-related CIP.
Journal:
Molecular Pain - MOL PAIN
, vol. 7, no. 1, pp. 1-15, 2011
DOI:
10.1186/1744-8069-7-32
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