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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2003-4-29
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pubmed:abstractText |
The basal conductance of unstimulated frog olfactory receptor neurons was investigated using whole-cell and perforated-patch recording. The input conductance, measured between -80 mV and -60 mV, averaged 0.25 nS in physiological saline. Studies were conducted to determine whether part of the input conductance is due to gating of neuronal cyclic-nucleotide-gated (CNG) channels. In support of this idea, the neuronal resting conductance was reduced by each of five treatments that reduce current through CNG channels: external application of divalent cations or amiloride; treatment with either of two adenylate cyclase inhibitors; and application of AMP-PNP, a competitive substrate for adenylate cyclase. The current blocked by divalent cations or by a cyclase inhibitor reversed near 0 mV, as expected for a CNG current. Under physiological conditions, gating of CNG channels contributes approximately 0.06 nS to the resting neuronal conductance. This implies a resting cAMP concentration of 0.1-0.3 micro M. A theoretical model suggests that a neuron containing 0.1-0.3 micro M cAMP is poised to give the largest possible depolarization in response to a very small olfactory stimulus. Although having CNG channels open at rest decreases the voltage change resulting from a given receptor current, it more substantially increases the receptor current resulting from a given increase in [cAMP].
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0006-3495
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
84
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3425-35
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:12719269-Adenylyl Imidodiphosphate,
pubmed-meshheading:12719269-Amiloride,
pubmed-meshheading:12719269-Animals,
pubmed-meshheading:12719269-Cells, Cultured,
pubmed-meshheading:12719269-Computer Simulation,
pubmed-meshheading:12719269-Cyclic Nucleotide-Gated Cation Channels,
pubmed-meshheading:12719269-Electric Conductivity,
pubmed-meshheading:12719269-Ion Channels,
pubmed-meshheading:12719269-Membrane Potentials,
pubmed-meshheading:12719269-Models, Neurological,
pubmed-meshheading:12719269-Olfactory Receptor Neurons,
pubmed-meshheading:12719269-Rana pipiens
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pubmed:year |
2003
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pubmed:articleTitle |
Contribution of cyclic-nucleotide-gated channels to the resting conductance of olfactory receptor neurons.
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pubmed:affiliation |
Department of Molecular and Cellular Physiology, University of Cincinnati, PO Box 670576, Cincinnati, OH 45267, USA. raymund.pun@uc.edu
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Evaluation Studies,
Validation Studies
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