Woodside B L, Borroni A M, Hammonds M D, Teyler T J
Department of Psychology, Baldwin-Wallace College, Berea, OH 44017, USA.
Neurobiol Learn Mem. 2004 Mar;81(2):105-14. doi: 10.1016/j.nlm.2003.10.003.
Activity dependent calcium entry into neurons can initiate a form of synaptic plasticity called long-term potentiation (LTP). This phenomenon is considered by many to be one possible cellular mechanism underlying learning and memory. The calcium entry that induces this phenomenon can occur when N-methyl-D-aspartate receptors (NMDARs) and/or voltage-dependent calcium channels (VDCCs) are activated. While much is known about synaptic plasticity and the mechanisms that are triggered by activation of these two Ca(2+) channels, it is unclear what roles they play in learning. To better understand the role activation of these channels may play in learning we systemically administered pharmacological antagonists to block NMDARs, VDCCs, or both during training trials and retention tests in a radial arm maze task. Wistar rats injected with the NMDAR antagonist MK-801 (0.1mg/kg) were impaired in the acquisition of this task. In contrast, rats injected with verapamil (10mg/kg), an antagonist to VDCCs, acquired the task at the same rate as control animals, but were impaired on a 10-day retention test. A group of animals injected with both antagonists were unable to learn the task. The results suggest that each of the calcium channels and the processes they trigger are involved in a different stage of memory formation or expression.
依赖活动的钙进入神经元可引发一种称为长时程增强（LTP）的突触可塑性形式。许多人认为这种现象是学习和记忆潜在的一种可能的细胞机制。当N-甲基-D-天冬氨酸受体（NMDARs）和/或电压依赖性钙通道（VDCCs）被激活时，可发生诱导这种现象的钙内流。虽然人们对突触可塑性以及由这两种Ca(2+)通道激活所触发的机制了解很多，但它们在学习中所起的作用尚不清楚。为了更好地理解这些通道的激活在学习中可能发挥的作用，我们在放射状臂迷宫任务的训练试验和保持测试期间，系统性地给予药理学拮抗剂以阻断NMDARs、VDCCs或两者。注射NMDAR拮抗剂MK-801（0.1mg/kg）的Wistar大鼠在该任务的习得方面受损。相比之下，注射维拉帕米（10mg/kg）（一种VDCCs拮抗剂）的大鼠以与对照动物相同的速率习得该任务，但在10天的保持测试中受损。一组注射了两种拮抗剂的动物无法学会该任务。结果表明，每个钙通道及其触发的过程都参与记忆形成或表达的不同阶段。
