Possible transsynaptic cholinergic neuromodulation by ATP released from ileal longitudinal muscles of guinea pigs
Autor: | Chiemi Sato, Tatsuo Furukawa, Katsuichi Matsuo, Takeo Tokunaga, Takeshi Katsuragi, Osamu Soejima, Katsuya Shirakabe |
---|---|
Rok vydání: | 1993 |
Předmět: |
Male
medicine.medical_specialty Guinea Pigs Neuromuscular transmission Alpha (ethology) In Vitro Techniques Biology General Biochemistry Genetics and Molecular Biology Neuromuscular junction Adenosine Triphosphate Ileum Neuromodulation Internal medicine medicine Animals Receptors Cholinergic General Pharmacology Toxicology and Pharmaceutics Adenosine Triphosphatases Muscle Smooth General Medicine Adenosine receptor Adenosine Acetylcholine medicine.anatomical_structure Endocrinology Synapses Cholinergic medicine.drug |
Zdroj: | Life Sciences. 53:911-918 |
ISSN: | 0024-3205 |
DOI: | 10.1016/0024-3205(93)90443-7 |
Popis: | The effects of alpha, beta-methylene ATP (alpha, beta-mATP) and beta, gamma-methylene ATP (beta, gamma-mATP) on endogenous acetylcholine (ACh) release evoked by electrical nerve stimulation were evaluated in guinea-pig ileal longitudinal muscles. Release of ACh was measured with an HPLC-electrochemical detector system and release of ATP by luciferin-luciferase assay. Electrically evoked endogenous ACh release was reduced by both alpha, beta-mATP and beta, gamma-mATP at concentrations of 3 and 30 microM. The inhibitory effect of alpha, beta-mATP (30 microM) on ACh release was not detectable in the presence of theophylline (100 microM), a P1-purinoceptor antagonist, that itself enhanced ATP release. When exogenous ATP (0.1 microM) was added to the bath in which the ileal segment was suspended, it was rapidly metabolized, presumably by ecto-ATPase, and disappeared from the medium within 15 min. At 30 microM, alpha, beta-mATP induced ATP release in a suramin-sensitive but Ca(2+)- and atropine-insensitive manner, suggesting P2-receptor-mediated release of ATP from the smooth muscle. We conclude from these findings that alpha, beta-mATP and, probably, also beta, gamma-mATP, do not reduce ACh release by direct stimulation of presynaptic P1-purinoceptors, and that endogenous ATP released postjunctionally by these ATP analogs is decomposed metabolically to adenosine in the synapse and this adenosine triggers P1-purinoceptor sensitive neuromodulation of cholinergic transmission. |
Databáze: | OpenAIRE |
Externí odkaz: |