Brănişteanu D, Schubert P, Brănişteanu D D
Physiologie. 1987 Jan-Mar;24(1):3-9.
In the hippocampal slice preparation of rats, preloaded with 3H-glutamate a local perfusion technique was used in order to measure the labelled transmitter output. The electrical receptive stimulation of the Schaffer collateral-commissural projections resulted in a detectable 3H-glutamate release which was significantly increased in the presence of 4-aminopyridine (4-AP). Exogenous adenosine and its analogue L-PIA induced a slight unsignificant reduction of the release while in the presence of 4-AP the release was almost completely blocked. Adding adenosine deaminase (ADA) did not change the normal transmitter release while in the presence of 4-AP the elimination of the endogenous adenosine brought about a significantly higher 3H-glutamate output. It is concluded that the adenosine-induced presynaptic inhibition of the transmitter release could be a significant mechanism under conditions in which the synaptic activity is abnormally high. This effect seems to be mediated via the A1 adenosine receptor since the D-PIA isomer application has no significant inhibitory effects.
在预先加载3H-谷氨酸的大鼠海马脑片制备中,采用局部灌注技术来测量标记递质的释放。对海马联合-连合投射进行电感受性刺激可导致可检测到的3H-谷氨酸释放,在4-氨基吡啶(4-AP)存在时,这种释放显著增加。外源性腺苷及其类似物L-PIA可引起释放略有不显著的减少,而在4-AP存在时,释放几乎完全被阻断。添加腺苷脱氨酶(ADA)不会改变正常递质释放,而在4-AP存在时,内源性腺苷的消除导致3H-谷氨酸输出显著增加。得出的结论是,在突触活动异常高的情况下,腺苷诱导的递质释放的突触前抑制可能是一种重要机制。这种作用似乎是通过A1腺苷受体介导的,因为应用D-PIA异构体没有显著的抑制作用。