Brain synaptosomes display a diadenosine tetraphosphate (Ap4A)‐mediated Ca2+ influx distinct from ATP‐mediated influx
Brain synaptosomes display a diadenosine tetraphosphate (Ap4A)‐mediated Ca2+ influx distinct from ATP‐mediated influx
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脑突触体表现出四磷酸二腺苷 (Ap4A) 介导的 Ca2+ 流入,与 ATP 介导的流入不同
DOI:
10.1002/(sici)1097-4547(19960601)44:5
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发表时间:
1996
影响因子:
4.2
通讯作者:
A. Nordone
中科院分区:
文献类型:
--
作者:
E. Pivorun;A. Nordone
Studies undertaken to compare the effects of Ap4A and ATP on altering intrasynaptosomal Ca2+ levels from deermouse brain reveal that both ligands induce a rapid influx of extracellular Ca2+. The Ca2+ profile elicited by 167 μM Ap4A is “spike‐like” (half‐time for decline to baseline, 19.1 ± 1.2 sec), in contrast to the gradual decline observed with ATP (104.0 ± 7.4 sec). DIDS (4‐4′‐diisothiocyano‐2,2′‐disulfonic acid stilbene) and suramin preincubation alter only the ATP‐induced Ca2+ profile. Cross‐desensitization studies indicate that prior application of ATP does not significantly affect the Ca2+ influx elicited by Ap4A, and that prior application of Ap4A does not affect the Ca2+ influx elicited by ATP. These results demonstrate that extracellular Ap4A and ATP elicit distinct intrasynaptosomal Ca2+ influx profiles, and suggest that these two nucleotides may be interacting with distinct purinoceptor subclasses or purinoceptor‐effector complexes. Subjecting the synaptosomes simultaneously to depolarization and Ap4A, or to depolarization and ATP, induces an additive effect on Ca2+ influx. Preincubation with verapamil negates the effects of depolarization without modifying the ligand‐elicited Ca2+ fluxes. These results indicate the presence of Ap4A and ATP ligand‐gated channels that may function as modulators of neuronal activity. © 1996 Wiley‐Liss, Inc.
DOI:
10.1007/978-1-4615-7305-0_5
发表时间:
1990
期刊:
Ion channels
影响因子:
--
作者:
Bean,BP;Friel,DD
通讯作者:
Friel,DD
DOI:
--
发表时间:
1988
期刊:
The Biochemical journal
影响因子:
--
作者:
McMillian,MK;Soltoff,SP;Lechleiter,JD;Cantley,LC;Talamo,BR
通讯作者:
Talamo,BR
影响因子:
2.9
作者:
Baker,JC;Jacobson,MK
通讯作者:
Jacobson,MK