TY - JOUR
T1 - The A1 agonist CCPA reduced bisoxonol-monitored membrane potential depolarization elicited by high K+ in cerebrocortical nerve endings
AU - Amoroso, Salvatore
AU - Iannotti, Elodia
AU - Saggese, Maria Luigia
AU - Di Renzo, Gianfranco
AU - Annunziato, Lucio
PY - 1995/10/4
Y1 - 1995/10/4
N2 - 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.
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.
KW - A-agonist activity
KW - Agonist
KW - Bisoxonol monitoring
KW - Cerebrocortical nerve ending
KW - Chlorocyclopentyladenosine
KW - Membrane potential
KW - Potassium ion
UR - http://www.scopus.com/inward/record.url?scp=0028981132&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028981132&partnerID=8YFLogxK
U2 - 10.1016/0005-2736(95)00143-Q
DO - 10.1016/0005-2736(95)00143-Q
M3 - Article
C2 - 7548146
AN - SCOPUS:0028981132
VL - 1239
SP - 67
EP - 73
JO - Biochimica et Biophysica Acta - Biomembranes
JF - Biochimica et Biophysica Acta - Biomembranes
SN - 0005-2736
IS - 1
ER -