HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Brown, P. Articles by Dale, N. Search for Related Content PubMed PubMed Citation Articles by Brown, P. Articles by Dale, N.

Adenosine A₁ receptors modulate high voltage-activated Ca²⁺ currents and motor pattern generation in the Xenopus embryo

Paul Brown and Nicholas Dale

1. Adenosine causes voltage- and non-voltage-dependent inhibition of high voltage-activated (HVA) Ca²⁺ currents in Xenopus laevis embryo spinal neurons.

2. As this inhibition can be blocked by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) and mimicked by N⁶-cyclopentyladenosine (CPA) it appears to be mediated by A₁ receptors. Agents active at A₂ receptors either were without effect or could be blocked by DPCPX. AMP had no agonist action on these receptors.

3. By using -conotoxin GVIA we found that adenosine inhibited an N-type Ca²⁺ current as well as a further unidentified HVA current that was insensitive to dihydropyridines, -agatoxin TK and -conotoxin MVIIC. Both types of current were subject to voltage- and non-voltage-dependent inhibition.

4. We used CPA and DPCPX to test whether A₁ 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 A₁ 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.