NDLI: Dual effects of adenosine on acetylcholine release from myenteric motoneurons are mediated by junctional facilitatory A2A and extrajunctional inhibitory A1 receptors

Content Provider	PubMed Central
Author	Margarida, Duarte-araújo Nascimento, Carlos Alexandrina, Timóteo M. Teresa, Magalhães-cardoso Paulo, Correia-de-sá
Copyright Year	2004
Abstract	The coexistence of both inhibitory A1 and facilitatory A2 adenosine receptors in the rat myenteric plexus prompted the question of how adenosine activates each receptor subtype to regulate cholinergic neurotransmission. Exogenously applied adenosine (0.3–300 μ M) decreased electrically evoked [3H]acetylcholine ([3H]ACh) release. Blocking A1 receptors with 1,3-dipropyl-8-cyclopentylxanthine (10 nM) transformed the inhibitory action of adenosine into a facilitatory effect. Adenosine-induced inhibition was mimicked by the A1 receptor agonist R-N 6 -phenylisopropyladenosine (0.3 μ M), but the A2A agonist CGS 21680C (0.003 μ M) produced a contrasting facilitatory effect. Increasing endogenous adenosine levels, by the addition of (1) the adenosine precursor AMP (30–100 μ M), (2) the adenosine kinase inhibitor 5′-iodotubercidin (10 μ M) or (3) inhibitors of adenosine uptake (dipyridamole, 0.5 μ M) and of deamination (erythro-9(2-hydroxy-3-nonyl)adenine, 50 μ M), enhanced electrically evoked [3H]ACh release (5 Hz for 40 s). Release facilitation was prevented by adenosine deaminase (ADA, 0.5 U ml−1) and by the A2A receptor antagonist ZM 241385 (50 nM); these compounds decreased [3H]ACh release by 31±6% (n=7) and 37±10% (n=6), respectively. Although inhibition of ecto-5′-nucleotidase by α,β-methylene ADP (200 μ M) or by concanavalin A (0.1 mg ml−1) attenuated endogenous adenosine formation from AMP, analysed by HPLC, the corresponding reduction in [3H]ACh release only became evident when stimulation of the myenteric plexus was prolonged to over 250 s. In summary, we found that endogenously generated adenosine plays a predominantly tonic facilitatory effect mediated by prejunctional A2A receptors. Extracellular deamination and cellular uptake may restrict endogenous adenosine actions to the neuro-effector region near the release/production sites.
Related Links	http://dx.doi.org/10.1038/sj.bjp.0705697
Ending Page	934
Page Count	10
Starting Page	925
File Format	PDF
ISSN	00071188
Journal	British Journal of Pharmacology
Issue Number	6
Volume Number	141
Language	English
Publisher Date	2004-03-01
Access Restriction	Open
Subject Keyword	Pharmacology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Pharmacology

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