腺苷A1受体介导的对诱发型谷氨酸释放的抑制作用与金鱼脑突触体中钙内流的减少相关联。

Adenosine A1 receptor-mediated inhibition of evoked glutamate release is coupled to calcium influx decrease in goldfish brain synaptosomes.

作者信息

Poli A, Lucchi R, Zottini M, Traversa U

机构信息

Department of Biology, Faculty of Sciences, University of Bologna, Italy.

出版信息

Brain Res. 1993 Aug 27;620(2):245-50. doi: 10.1016/0006-8993(93)90162-g.

DOI:10.1016/0006-8993(93)90162-g

PMID:8103701

Abstract

Binding of [3H]cyclohexyladenosine (CHA) to the cellular fractions and P2 subfractions of the goldfish brain was studied. The A1 receptor density was predominantly in synaptosomal membranes. In goldfish brain synaptosomes (P2), 30 mM K+ stimulated glutamate, taurine and GABA release in a Ca(2+)-dependent fashion, whereas the aspartate release was Ca(2+)-independent. Adenosine, R-phenylisopropyladenosine (R-PIA) and CHA (100 microM) inhibited K(+)-stimulated glutamate release (31%, 34% and 45%, respectively). All of these effects were reversed by the selective adenosine A1 receptor antagonist, 8-cyclopentyltheophylline (CPT). In the same synaptosomal preparation, K+ (30 mM) stimulated Ca2+ influx (46.8 +/- 6.8%) and this increase was completely abolished by pretreatment with 100 nM omega-conotoxin. Pretreatment with 100 microM R-PIA or 100 microM CHA, reduced the evoked increase of intra-synaptosomal Ca2+ concentration, respectively by 37.7 +/- 4.3% and 39.7 +/- 9.0%. A possible correlation between presynaptic A1 receptor inhibition of glutamate release and inhibition of calcium influx is discussed.

摘要

研究了[³H]环己基腺苷（CHA）与金鱼脑的细胞组分和P2亚组分的结合情况。A1受体密度主要存在于突触体膜中。在金鱼脑突触体（P2）中，30 mM K⁺以Ca²⁺依赖的方式刺激谷氨酸、牛磺酸和GABA释放，而天冬氨酸释放则不依赖Ca²⁺。腺苷、R-苯异丙基腺苷（R-PIA）和CHA（100 μM）抑制K⁺刺激的谷氨酸释放（分别为31%、34%和45%）。所有这些作用都被选择性腺苷A1受体拮抗剂8-环戊基茶碱（CPT）逆转。在相同的突触体制备中，K⁺（30 mM）刺激Ca²⁺内流（46.8±6.8%），而用100 nM ω-芋螺毒素预处理可完全消除这种增加。用100 μM R-PIA或100 μM CHA预处理分别使诱发的突触体内Ca²⁺浓度增加降低37.7±4.3%和39.7±9.0%。讨论了突触前A1受体对谷氨酸释放的抑制与钙内流抑制之间可能的相关性。