de Mendonça A, Almeida T, Bashir Z I, Ribeiro J A
Laboratory of Pharmacology, Gulbenkian Institute of Science, Oeiras, Portugal.
Neuropharmacology. 1997 Feb;36(2):161-7. doi: 10.1016/s0028-3908(96)00173-6.
This study tested the hypothesis that endogenous adenosine, a neuromodulator which is known to modify long-term potentiation (LTP), might also affect other forms of long-lasting synaptic plasticity, namely long-term depression (LTD) and depotentiation, in the hippocampus. Long-term depression was induced by applying low-frequency stimulation (LFS; 1 Hz, 900 stimuli, test intensity) to the Schaffer collateral-commissural fibres in hippocampal slices taken from young (12-14-day old) animals. Depotentiation was induced by delivering LFS to a pathway in which LTP had previously been saturated. Under control conditions, LTD induced in two distinct pathways was similar. However, low-frequency stimulation, applied in either pathway in the presence of the selective adenosine A1 receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX; 10 nM), resulted in LTD which was larger than in control conditions. In a similar way, while under control conditions depotentiation induced in two distinct pathways was similar, when LFS was applied in the presence of DPCPX (10 nM) facilitation of depotentiation was observed. These results suggest that endogenous adenosine, acting through adenosine A1 receptors, is able to attenuate long-term depression and depotentiation in the hippocampus.
内源性腺苷作为一种已知可调节长时程增强（LTP）的神经调质，可能也会影响海马体中其他形式的持久突触可塑性，即长时程抑制（LTD）和去增强作用。通过对取自幼年（12 - 14日龄）动物的海马体切片中的Schaffer侧支 - 连合纤维施加低频刺激（LFS；1 Hz，900次刺激，测试强度）来诱导长时程抑制。通过向先前LTP已饱和的通路传递LFS来诱导去增强作用。在对照条件下，在两条不同通路中诱导的LTD相似。然而，在存在选择性腺苷A1受体拮抗剂1,3 - 二丙基 - 8 - 环戊基黄嘌呤（DPCPX；10 nM）的情况下，在任一条通路中施加低频刺激，所产生的LTD都比对照条件下更大。同样，在对照条件下，在两条不同通路中诱导的去增强作用相似，但当在存在DPCPX（10 nM）的情况下施加LFS时，观察到去增强作用得到促进。这些结果表明，内源性腺苷通过腺苷A1受体发挥作用，能够减弱海马体中的长时程抑制和去增强作用。
