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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Kimura, M. Kimura, I. Tsuneki, H. Dezaki, K. |
| Description | Author Affiliation: Kimura I ( Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University, Japan.) |
| Abstract | 1. The involvement of calcitonin gene-related peptide (CGRP) in the mechanism of nicotinic acetylcholine receptor-operated noncontractile Ca2+ mobilization (not accompanied by twitch tension) was investigated by measuring Ca(2+)-aequorin luminescence at the neuromuscular junction of mouse diaphragm muscle treated with neostigmine. 2. Noncontractile Ca2+ transients were enhanced by 4-aminopyridine (100 microM), a K+ channel blocker, and inhibited by botulinum toxin (1-100 micrograms, i.p.) and hexamethonium (10-100 microM), a neuronal nicotinic receptor antagonist. 3. Noncontractile Ca2+ transients were diminished by CGRP8-37 (10-20 microM), a CGRP antagonist. CGRP (0.3-10 nM) prolonged the duration of noncontractile Ca2+ transients. The effect of CGRP was suppressed by CGRP8-37 (0.1 microM). 4. Noncontractile Ca2+ transients were inhibited by H-89 (0.1-1 microM), a protein kinase-A inhibitor. The catalytic subunit of protein kinase-A and AA373 (300 microM), a protein kinase-A activator, prolonged the duration of noncontractile transients. The prolongations either by CGRP or by AA373 were not observed in the presence of H-89 (0.1 microM). 5. Contractile (accompanied by twitch tension) but not noncontractile Ca2+ transients were decreased by 12-O-tetradecanoyl phorbol 13-acetate (TPA, 0.3-1 microM), a protein kinase-C activator. Phospholipase A2 increased only contractile Ca2+ transients. Calmodulin-related agents affected neither type of Ca2+ transients. 6. These results provide the first evidence that nicotinic acetylcholine receptor-operated noncontractile Ca2+ mobilization is promoted by nerve-released CGRP activating protein kinase-A, and is dependent on the accumulated amounts of acetylcholine at the neuromuscular junction where desensitization might readily develop. |
| ISSN | 00071188 |
| e-ISSN | 14765381 |
| Journal | British Journal of Pharmacology |
| Issue Number | 2 |
| Volume Number | 110 |
| Language | English |
| Publisher | Wiley Online Library(on behalf of The British Pharmacological Society) |
| Publisher Date | 1993-10-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Calcitonin Gene-Related Peptide Pharmacology Calcium Metabolism Neuromuscular Junction Receptors, Nicotinic Drug Effects Acetylcholine Physiology Animals Calmodulin Cyclic AMP Cyclic AMP-Dependent Protein Kinases Enzyme Activation In Vitro Techniques Mice Mice, Inbred Strains Muscle Contraction Nerve Endings Enzymology Phospholipases A Phospholipases A2 Protein Kinase C Receptors, Presynaptic Signal Transduction Research Support, Non-U.S. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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