| Effects of ATP and derivatives on neuropile glial cells of the leech central nervous system. | |
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MedLine Citation:
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PMID: 10642746 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We investigated the effects of ATP (adenosine 5'-triphosphate) and derivatives on leech neuropile glial cells, focusing on exposed glial cells. ATP dose-dependently depolarized or hyperpolarized neuropile glial cells in situ as well as exposed neuropile glial cells. These potential shifts varied among cells and repetitive ATP application did not change their amplitude, duration or direction. In exposed neuropile glial cells, ATP most frequently induced a Na(+)-dependent depolarization and decreased the input resistance. The agonist potency ATP > ADP (adenosine 5'-diphosphate) > AMP (adenosine 5'-monophosphate) > adenosine indicates that P2 purinoceptors mediate this depolarization. The P2Y agonist 2-methylthio-ATP mimicked the ATP-induced depolarization, whereas the P2Y antagonist PPADS (pyridoxal-phosphate-6-azophenyl-2', 4'-disulphonic acid) reduced it. P2X agonists were without effect. Because the P1 antagonist 8-SPT (8-(p-sulphophenyl)-theophylline) also depressed ATP-induced depolarizations and some ATP-insensitive glial cells responded to adenosine, we suggest coexpression of metabotropic P2Y and P1 purinoceptors. The ATP-induced depolarization requires activation of Na(+) channels or nonselective cation channels, whereas the ATP-induced hyperpolarization indicates activation of K(+) channels. ATP also increased the intracellular Ca(2+) concentration ([Ca(2+)](i)), that is independent of Ca(2+) influx but reflects intracellular Ca(2+) release possibly triggered by IP(3) formation. ADP and AMP also increased [Ca(2+)](i), but were less efficient than ATP; adenosine and 2-methylthio-ATP did not affect [Ca(2+)](i). In view of the mobilization of intracellular Ca(2+), ATP is clearly different from other leech neurotransmitters, because it enables intracellular Ca(2+) signaling without causing prominent changes in glial membrane potential. Thus disturbance of the extracellular microenvironment and the demand for metabolic energy are minimized. |
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Authors:
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M Müller; A Henrich; J Klockenhoff; P W Dierkes; W R Schlue |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Glia Volume: 29 ISSN: 0894-1491 ISO Abbreviation: Glia Publication Date: 2000 Feb |
Date Detail:
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Created Date: 2000-02-17 Completed Date: 2000-02-17 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8806785 Medline TA: Glia Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 191-201 Citation Subset: IM |
Copyright Information:
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Copyright 2000 Wiley-Liss, Inc. |
Affiliation:
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Institut für Neurobiologie, Heinrich-Heine-Universität Düsseldorf, Universitätsstrasse 1, Düsseldorf, Germany. m.mueller@cellbio.duke.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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analogs & derivatives*,
pharmacology* Animals Cations, Divalent / pharmacology Cell Membrane / drug effects Central Nervous System / cytology, drug effects*, physiology Electrophysiology Ions Leeches / drug effects*, physiology Neuroglia / drug effects*, metabolism, physiology Neuropil / cytology, drug effects*, physiology Purines / pharmacology Pyrimidines / pharmacology Receptors, Glutamate / drug effects Receptors, Nicotinic / drug effects Receptors, Purinergic / agonists, antagonists & inhibitors, classification |
| Chemical | |
Reg. No./Substance:
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0/Cations, Divalent; 0/Ions; 0/Purines; 0/Pyrimidines; 0/Receptors, Glutamate; 0/Receptors, Nicotinic; 0/Receptors, Purinergic; 56-65-5/Adenosine Triphosphate |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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