D1/D5多巴胺受体通过环磷酸腺苷（cAMP）依赖性机制抑制海马体CA1区突触的去增强作用。
D1/D5 dopamine receptors inhibit depotentiation at CA1 synapses via cAMP-dependent mechanism.
作者信息
Otmakhova N A, Lisman J E
机构信息
Department of Biology and Volen Center for Complex Systems, Brandeis University, Waltham, Massachusetts 02254, USA.
出版信息
J Neurosci. 1998 Feb 15;18(4):1270-9. doi: 10.1523/JNEUROSCI.18-04-01270.1998.
Abstract
Recent work has shown that D1/D5 dopamine receptors can enhance long-term potentiation (LTP). We investigated whether D1/D5 receptors also affect depotentiation, the reversal of LTP by low-frequency stimulation. D1/D5 agonists greatly reduced depotentiation, an effect that was inhibited by a D1/D5 antagonist. The D1/D5 effect appears to be mediated by adenylyl cyclase (AC) and cAMP-dependent protein kinase (PKA), because it was mimicked by the AC activator forskolin and was inhibited by the AC and PKA inhibitors. In vivo studies show that dopamine is released when a reward occurs. Our results raise the possibility that the memory of events before reward might be retained selectively, because dopamine blocks their erasure.
摘要
近期研究表明，D1/D5多巴胺受体可增强长时程增强效应（LTP）。我们研究了D1/D5受体是否也会影响去增强作用，即通过低频刺激使LTP逆转。D1/D5激动剂可显著减少去增强作用，该效应可被D1/D5拮抗剂抑制。D1/D5的作用似乎是由腺苷酸环化酶（AC）和环磷酸腺苷依赖性蛋白激酶（PKA）介导的，因为它可被AC激活剂福斯高林模拟，并被AC和PKA抑制剂抑制。体内研究表明，当奖励出现时多巴胺会释放。我们的研究结果提出了一种可能性，即奖励之前事件的记忆可能会被选择性保留，因为多巴胺会阻止这些记忆的消除。
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