The A1 agonist CCPA reduced bisoxonol-monitored membrane potential depolarization elicited by high K+ in cerebrocortical nerve endings

Salvatore Amoroso, Elodia Iannotti, Maria Luigia Saggese, Gianfranco Di Renzo, Lucio Annunziato

Research output: Contribution to journal › Article

Abstract

In this study the effect of the A1 agonist 2-chloro-N6-cyclopentyladenosine (CCPA) on bis(1,3-diethylthiobarbituric acid) trimethine oxonol (bisoxonol)-monitored membrane potential in cerebrocortical nerve endings was evaluated. CCPA (30, 100 and 300 μM) caused a dose-dependent decrease of high K+- and veratridine-induced membrane depolarization. This decrease was counteracted by the A1-specific antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) (30-100 μM). On the contrary, the A2 receptor antagonist 9-chloro-2-(2-furanyl)-5,6-dihydro-1,2,4-triazolol-[1,5-c]quinazoline-5-imine (CGS 15943) was unable to interface with the lowering effect exerted by CCPA (100 μM) on K+-elicited membrane depolarization. Finally, the A2 receptor agonist 2-[p-(2-carboxyl-ethyl)phenethylamine]-5′-N-ethylcarboxamidoadenosine (CGS 21680) did not induce any modification of K+-induced membrane depolarization. The results of the present study suggest that K+-induced membrane depolarization in cerebrocortical brain nerve endings may be modulated by A1 receptors.

Original languageEnglish
Pages (from-to)67-73
Number of pages7
JournalBBA - Biomembranes
Volume1239
Issue number1
DOIs
Publication statusPublished - Oct 4 1995

Fingerprint

Nerve Endings
Depolarization
Membrane Potentials
Membranes
varespladib methyl
Adenosine-5'-(N-ethylcarboxamide)
Quinazolines
Veratridine
Imines
Brain
Acids
N(6)-cyclopentyladenosine

Keywords

  • A-agonist activity
  • Agonist
  • Bisoxonol monitoring
  • Cerebrocortical nerve ending
  • Chlorocyclopentyladenosine
  • Membrane potential
  • Potassium ion

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology

Cite this

The A1 agonist CCPA reduced bisoxonol-monitored membrane potential depolarization elicited by high K+ in cerebrocortical nerve endings. / Amoroso, Salvatore; Iannotti, Elodia; Saggese, Maria Luigia; Di Renzo, Gianfranco; Annunziato, Lucio.

In: BBA - Biomembranes, Vol. 1239, No. 1, 04.10.1995, p. 67-73.

Research output: Contribution to journal › Article

Amoroso, S, Iannotti, E, Saggese, ML, Di Renzo, G & Annunziato, L 1995, 'The A1 agonist CCPA reduced bisoxonol-monitored membrane potential depolarization elicited by high K+ in cerebrocortical nerve endings', BBA - Biomembranes, vol. 1239, no. 1, pp. 67-73. https://doi.org/10.1016/0005-2736(95)00143-Q
Amoroso S, Iannotti E, Saggese ML, Di Renzo G, Annunziato L. The A1 agonist CCPA reduced bisoxonol-monitored membrane potential depolarization elicited by high K+ in cerebrocortical nerve endings. BBA - Biomembranes. 1995 Oct 4;1239(1):67-73. https://doi.org/10.1016/0005-2736(95)00143-Q
Amoroso, Salvatore ; Iannotti, Elodia ; Saggese, Maria Luigia ; Di Renzo, Gianfranco ; Annunziato, Lucio. / The A1 agonist CCPA reduced bisoxonol-monitored membrane potential depolarization elicited by high K+ in cerebrocortical nerve endings. In: BBA - Biomembranes. 1995 ; Vol. 1239, No. 1. pp. 67-73.
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AB - In this study the effect of the A1 agonist 2-chloro-N6-cyclopentyladenosine (CCPA) on bis(1,3-diethylthiobarbituric acid) trimethine oxonol (bisoxonol)-monitored membrane potential in cerebrocortical nerve endings was evaluated. CCPA (30, 100 and 300 μM) caused a dose-dependent decrease of high K+- and veratridine-induced membrane depolarization. This decrease was counteracted by the A1-specific antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) (30-100 μM). On the contrary, the A2 receptor antagonist 9-chloro-2-(2-furanyl)-5,6-dihydro-1,2,4-triazolol-[1,5-c]quinazoline-5-imine (CGS 15943) was unable to interface with the lowering effect exerted by CCPA (100 μM) on K+-elicited membrane depolarization. Finally, the A2 receptor agonist 2-[p-(2-carboxyl-ethyl)phenethylamine]-5′-N-ethylcarboxamidoadenosine (CGS 21680) did not induce any modification of K+-induced membrane depolarization. The results of the present study suggest that K+-induced membrane depolarization in cerebrocortical brain nerve endings may be modulated by A1 receptors.

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