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Adenosine A 1 receptors modulate high voltage‐activated Ca 2+ currents and motor pattern generation in the Xenopus embryo
Author(s) -
Brown Paul,
Dale Nicholas
Publication year - 2000
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2000.00655.x
Subject(s) - adenosine , adenosine a1 receptor , receptor , xenopus , agonist , adenosine receptor , medicine , endocrinology , biology , neuroscience , motor neuron , chemistry , pharmacology , microbiology and biotechnology , biophysics , biochemistry , spinal cord , gene
1 Adenosine causes voltage‐ and non‐voltage‐dependent inhibition of high voltage‐activated (HVA) Ca 2+ currents in Xenopus laevis embryo spinal neurons. 2 As this inhibition can be blocked by 8‐cyclopentyl‐1,3‐dipropylxanthine (DPCPX) and mimicked by N 6 ‐cyclopentyladenosine (CPA) it appears to be mediated by A 1 receptors. Agents active at A 2 receptors either were without effect or could be blocked by DPCPX. AMP had no agonist action on these receptors. 3 By using ω‐conotoxin GVIA we found that adenosine inhibited an N‐type Ca 2+ current as well as a further unidentified HVA current that was insensitive to dihydropyridines, ω‐agatoxin TK and ω‐conotoxin MVIIC. Both types of current were subject to voltage‐ and non‐voltage‐dependent inhibition. 4 We used CPA and DPCPX to test whether A 1 receptors regulated spinal motor pattern generation in spinalized Xenopus embryos. DPCPX caused a near doubling of, while CPA greatly shortened, the length of swimming episodes. In addition, DPCPX slowed, while CPA greatly speeded up, the rate of run‐down of motor activity. 5 Our results demonstrate a novel action of A 1 receptors in modulating spinal motor activity. Furthermore they confirm that adenosine is produced continually throughout swimming episodes and acts to cause the eventual termination of activity.