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Adenosine inhibits N‐type calcium channels at the rat neuromuscular junction
Author(s) -
Schwartz Andrew D,
Whitacre Camron L,
Lin Yue,
Wilson David F
Publication year - 2003
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.2003.03806.x
Subject(s) - adenosine , l type calcium channel , neuromuscular junction , calcium , adenosine receptor , voltage dependent calcium channel , t type calcium channel , chemistry , inhibitory postsynaptic potential , calcium channel , medicine , adenosine a1 receptor , endocrinology , calcium in biology , pharmacology , receptor , biology , neuroscience , agonist
Summary 1. In earlier studies, it has been reported that under in vitro conditions transmitter release at the rat neuromuscular junction is normally suppressed due to the effect of adenosine release from the isolated tissue. In the present study we wanted to determine whether this action may involve the inhibition of calcium influx through adenosine‐sensitive calcium channels. 2. In order to test this hypothesis, we examined the role of N‐type calcium channels in regulating nerve‐evoked transmitter release by using the N‐type calcium channel‐specific blocker ω‐conotoxin GVIA (CTX). In order to control the inhibitory action of adenosine, we also used the adenosine A 1 receptor antagonist 1,3‐dipropyl‐8‐cyclopentylxanthine (DPCPX). We tested the effect of blocking N‐type calcium channels with CTX in the presence and absence of DPCPX. We examined the effects of these drugs on quantal transmitter release in the transected preparation of the phrenic nerve–hemidiaphragm of the rat using intracellular recording techniques. 3. At 10 nmol/L, CTX alone had no effect on nerve‐evoked transmitter release; however, in the presence of 0.1 µmol/L DPCPX, CTX significantly depressed nerve‐evoked transmitter release. 4. These data support the view that adenosine inhibits nerve‐evoked transmitter release by inhibiting N‐type calcium channels on nerve terminals.