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Adenosine A(1) receptors modulate high voltage-activated Ca2+ currents and motor pattern generation in the Xenopus embryo

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UNSPECIFIED (2000) Adenosine A(1) receptors modulate high voltage-activated Ca2+ currents and motor pattern generation in the Xenopus embryo. JOURNAL OF PHYSIOLOGY-LONDON, 525 (3). pp. 655-667.

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Abstract

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 N-6-cyclopentyladenosine (CPA) it appears to be mediated by A(1) receptors. Agents active at A, receptors either were without effect or could be blocked by DPCPX. AMP had no agonist action on these receptors.

3. By using omega-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, omega-agatoxin TK and omega-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.

Item Type: Journal Article
Subjects: R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Q Science > QP Physiology
Journal or Publication Title: JOURNAL OF PHYSIOLOGY-LONDON
Publisher: CAMBRIDGE UNIV PRESS
ISSN: 0022-3751
Official Date: 15 June 2000
Dates:
DateEvent
15 June 2000UNSPECIFIED
Volume: 525
Number: 3
Number of Pages: 13
Page Range: pp. 655-667
Publication Status: Published

Data sourced from Thomson Reuters' Web of Knowledge

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