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Adenosine A/sub 1/R receptor deficiency enhances hippocampal long-term potentiation in freely moving mice

机译:腺苷A / sub 1 / R受体缺乏会增强自由移动小鼠的海马长时程增强

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This paper addresses the role of adenosine A/sub 1/R receptors (A/sub 1/R) on synaptic efficacy in the hippocampus. Adenosine A/sub 1/ receptors (A/sub 1/R) have known inhibitory effects in the CNS by both hyperpolarizing neurons and inhibiting Ca/sup 2+/ influx. This inhibitory effect leads to a decrease in glutamate release. Glutamate, in turn, activates NMDA receptors, which is thought to lead to long-term potentiation (LTP). Thus, we hypothesized that elimination of A/sub 1/R's would lead to an increase in both NMDA activation and LTP. To assess the role of adenosine on synaptic plasticity in the hippocampus, LTP was induced in freely moving wild type (normal) and A/sub 1/R knockout (KO) mice, which lack the gene coding for the A/sub 1/R. Preliminary results show that LTP is enhanced in KO mice compared to controls, which corresponds to the inhibitory effects of adenosine.
机译:本文探讨了腺苷A / sub 1 / R受体(A / sub 1 / R)对海马突触功效的作用。腺苷A / sub 1 /受体(A / sub 1 / R)通过使神经元超极化并抑制Ca / sup 2 + /涌入,在中枢神经系统中具有已知的抑制作用。这种抑制作用导致谷氨酸盐释放的减少。谷氨酸反过来会激活NMDA受体,这被认为会导致长期增强(LTP)。因此,我们假设消除A / sub 1 / R将导致NMDA激活和LTP的增加。为了评估腺苷在海马突触可塑性中的作用,在自由运动的野生型(正常)和A / sub 1 / R基因敲除(KO)小鼠中诱导了LTP,它们缺乏编码A / sub 1 / R的基因。初步结果表明,与对照组相比,KO小鼠的LTP增强,这与腺苷的抑制作用相对应。

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