Abstract
Degenerin/ epithelial Na + channels (DEG/ENaCs) are voltage-independent Na + or Na +/Ca 2+ channels expressed in many tissues and are needed for a wide range of physiological functions, including sensory perception and transepithelial Na + transport. In the nervous system, DEG/ENaCs are expressed in both neurons and glia. However, the role of glial vs. neuronal DEG/ENaCs remains unclear. We recently reported the characterization of a novel DEG/ENaC in Caenorhabditis elegans that we named ACD-1. ACD-1 is expressed in glial amphid sheath cells. The glial ACD-1, together with the neuronal DEG/ENaC DEG-1, is necessary for acid avoidance and attraction to lysine. We report presently that knockout of acd-1 in glia exacerbates sensory deficits caused by another mutant: the hypomorphic allele of the cGMP-gated channel subunit tax-2. Furthermore, sensory deficits caused by mutations in Gi protein odr-3 and guanylate cyclase daf-11, which regulate the activity of TAX-2/TAX-4 channels, are worsened by knockout of acd-1. We also show that sensory neurons of acd-1 tax-2(p694) double mutants fail to undergo changes in intracellular Ca 2+ when animals are exposed to low concentrations of attractant. Finally, we show that exogenous expression of TRPV1 in sensory neurons and exposure to capsaicin rescue sensory deficits of acd-1 tax-2(p694) mutants, suggesting that sensory deficits of these mutants are bypassed by increasing neuronal excitability. Our data suggest a role of glial DEG/ENaC channel ACD-1 in supporting neuronal activity.
| Original language | English |
|---|---|
| Pages (from-to) | 148-158 |
| Number of pages | 11 |
| Journal | Journal of Neurophysiology |
| Volume | 107 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jan 1 2012 |
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Keywords
- Chemotaxis
- Degenerin/epithelial sodium channel
- Imaging
ASJC Scopus subject areas
- Physiology
- Neuroscience(all)
Cite this
Knockout of glial channel ACD-1 exacerbates sensory deficits in a C. elegans mutant by regulating calcium levels of sensory neurons. / Wang, Ying; D'Urso, Giulia; Bianchi, Laura.
In: Journal of Neurophysiology, Vol. 107, No. 1, 01.01.2012, p. 148-158.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Knockout of glial channel ACD-1 exacerbates sensory deficits in a C. elegans mutant by regulating calcium levels of sensory neurons
AU - Wang, Ying
AU - D'Urso, Giulia
AU - Bianchi, Laura
PY - 2012/1/1
Y1 - 2012/1/1
N2 - Degenerin/ epithelial Na + channels (DEG/ENaCs) are voltage-independent Na + or Na +/Ca 2+ channels expressed in many tissues and are needed for a wide range of physiological functions, including sensory perception and transepithelial Na + transport. In the nervous system, DEG/ENaCs are expressed in both neurons and glia. However, the role of glial vs. neuronal DEG/ENaCs remains unclear. We recently reported the characterization of a novel DEG/ENaC in Caenorhabditis elegans that we named ACD-1. ACD-1 is expressed in glial amphid sheath cells. The glial ACD-1, together with the neuronal DEG/ENaC DEG-1, is necessary for acid avoidance and attraction to lysine. We report presently that knockout of acd-1 in glia exacerbates sensory deficits caused by another mutant: the hypomorphic allele of the cGMP-gated channel subunit tax-2. Furthermore, sensory deficits caused by mutations in Gi protein odr-3 and guanylate cyclase daf-11, which regulate the activity of TAX-2/TAX-4 channels, are worsened by knockout of acd-1. We also show that sensory neurons of acd-1 tax-2(p694) double mutants fail to undergo changes in intracellular Ca 2+ when animals are exposed to low concentrations of attractant. Finally, we show that exogenous expression of TRPV1 in sensory neurons and exposure to capsaicin rescue sensory deficits of acd-1 tax-2(p694) mutants, suggesting that sensory deficits of these mutants are bypassed by increasing neuronal excitability. Our data suggest a role of glial DEG/ENaC channel ACD-1 in supporting neuronal activity.
AB - Degenerin/ epithelial Na + channels (DEG/ENaCs) are voltage-independent Na + or Na +/Ca 2+ channels expressed in many tissues and are needed for a wide range of physiological functions, including sensory perception and transepithelial Na + transport. In the nervous system, DEG/ENaCs are expressed in both neurons and glia. However, the role of glial vs. neuronal DEG/ENaCs remains unclear. We recently reported the characterization of a novel DEG/ENaC in Caenorhabditis elegans that we named ACD-1. ACD-1 is expressed in glial amphid sheath cells. The glial ACD-1, together with the neuronal DEG/ENaC DEG-1, is necessary for acid avoidance and attraction to lysine. We report presently that knockout of acd-1 in glia exacerbates sensory deficits caused by another mutant: the hypomorphic allele of the cGMP-gated channel subunit tax-2. Furthermore, sensory deficits caused by mutations in Gi protein odr-3 and guanylate cyclase daf-11, which regulate the activity of TAX-2/TAX-4 channels, are worsened by knockout of acd-1. We also show that sensory neurons of acd-1 tax-2(p694) double mutants fail to undergo changes in intracellular Ca 2+ when animals are exposed to low concentrations of attractant. Finally, we show that exogenous expression of TRPV1 in sensory neurons and exposure to capsaicin rescue sensory deficits of acd-1 tax-2(p694) mutants, suggesting that sensory deficits of these mutants are bypassed by increasing neuronal excitability. Our data suggest a role of glial DEG/ENaC channel ACD-1 in supporting neuronal activity.
KW - Chemotaxis
KW - Degenerin/epithelial sodium channel
KW - Imaging
UR - http://www.scopus.com/inward/record.url?scp=84255167330&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84255167330&partnerID=8YFLogxK
U2 - 10.1152/jn.00299.2011
DO - 10.1152/jn.00299.2011
M3 - Article
C2 - 21994266
AN - SCOPUS:84255167330
VL - 107
SP - 148
EP - 158
JO - Journal of Neurophysiology
JF - Journal of Neurophysiology
SN - 0022-3077
IS - 1
ER -