Source:http://linkedlifedata.com/resource/pubmed/id/17928563
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
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| pubmed:dateCreated |
2007-12-21
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| pubmed:abstractText |
Learning and memory are critically dependent on basal forebrain cholinergic (BFC) neuron excitability, which is modulated profoundly by leak K(+) channels. Many neuromodulators closing leak K(+) channels have been reported, whereas their endogenous opener remained unknown. We here demonstrate that nitric oxide (NO) can be the endogenous opener of leak K(+) channels in the presumed BFC neurons. Bath application of 1 mM S-nitroso-N-acetylpenicillamine (SNAP), an NO donor, induced a long-lasting hyperpolarization, which was often interrupted by a transient depolarization. Soluble guanylyl cyclase inhibitors prevented SNAP from inducing hyperpolarization but allowed SNAP to cause depolarization, whereas bath application of 0.2 mM 8-bromoguanosine-3',5'-cyclomonophosphate (8-Br-cGMP) induced a similar long-lasting hyperpolarization alone. These observations indicate that the SNAP-induced hyperpolarization and depolarization are mediated by the cGMP-dependent and -independent processes, respectively. When examined with the ramp command pulse applied at -70 mV under the voltage-clamp condition, 8-Br-cGMP application induced the outward current that reversed at K(+) equilibrium potential (E(K)) and displayed Goldman-Hodgkin-Katz rectification, indicating the involvement of voltage-independent K(+) current. By contrast, SNAP application in the presumed BFC neurons either dialyzed with the GTP-free internal solution or in the presence of 10 muM Rp-8-bromo-beta-phenyl-1,N(2)-ethenoguanosine 3',5'-cyclic monophosphorothioate sodium salt, a protein kinase G (PKG) inhibitor, induced the inward current that reversed at potentials much more negative than E(K) and close to the reversal potential of Na(+)-K(+) pump current. These observations strongly suggest that NO activates leak K(+) channels through cGMP-PKG-dependent pathway to markedly decrease the excitability in BFC neurons, while NO simultaneously causes depolarization by the inhibition of Na(+)-K(+) pump through ATP depletion.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Barium,
http://linkedlifedata.com/resource/pubmed/chemical/Cesium,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic GMP,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic GMP-Dependent Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Fluorescent Dyes,
http://linkedlifedata.com/resource/pubmed/chemical/Guanylate Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Donors,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/S-Nitroso-N-Acetylpenicillamine,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Potassium-Exchanging ATPase
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| pubmed:status |
MEDLINE
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| pubmed:month |
Dec
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| pubmed:issn |
0022-3077
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
98
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
3397-410
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:17928563-Adenosine Triphosphate,
pubmed-meshheading:17928563-Animals,
pubmed-meshheading:17928563-Barium,
pubmed-meshheading:17928563-Cesium,
pubmed-meshheading:17928563-Cyclic GMP,
pubmed-meshheading:17928563-Cyclic GMP-Dependent Protein Kinases,
pubmed-meshheading:17928563-Data Interpretation, Statistical,
pubmed-meshheading:17928563-Electrophysiology,
pubmed-meshheading:17928563-Female,
pubmed-meshheading:17928563-Fluorescent Dyes,
pubmed-meshheading:17928563-Guanylate Cyclase,
pubmed-meshheading:17928563-Male,
pubmed-meshheading:17928563-Neurons,
pubmed-meshheading:17928563-Nitric Oxide,
pubmed-meshheading:17928563-Nitric Oxide Donors,
pubmed-meshheading:17928563-Parasympathetic Nervous System,
pubmed-meshheading:17928563-Patch-Clamp Techniques,
pubmed-meshheading:17928563-Potassium Channels,
pubmed-meshheading:17928563-Prosencephalon,
pubmed-meshheading:17928563-Rats,
pubmed-meshheading:17928563-Rats, Wistar,
pubmed-meshheading:17928563-S-Nitroso-N-Acetylpenicillamine,
pubmed-meshheading:17928563-Sodium-Potassium-Exchanging ATPase
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| pubmed:year |
2007
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| pubmed:articleTitle |
Nitric oxide activates leak K+ currents in the presumed cholinergic neuron of basal forebrain.
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| pubmed:affiliation |
Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, Suita, Osaka, Japan. kang@dent.osaka-u.ac.jp
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| pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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