Mechanisms influencing acquisition and recall of motor memories
Mechanisms influencing acquisition and recall of motor memories
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DOI：
10.1152/jn.2002.88.4.2114
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发表时间：
2002-10-01
影响因子：
2.5
通讯作者：
Shadmehr, R
中科院分区：
文献类型：
--
作者：
Donchin, O;Sawaki, L;Shadmehr, R
工具或物体动力学的内部模型是学习使用工具或操纵物体时获得的运动记忆的一部分。突触功效的变化可能是记忆获取和存储的基础。在这里，我们研究了干扰突触可塑性的药物对新运动记忆的获得和对先前学习的内部模型的回忆的影响。分为六组的四十九名受试者，在握住机械臂并向手施加力的同时进行伸手动作。第一天，所有受试者学会在力场 A 中移动。第二天，测试每组受试者回忆 A 场的能力和学习 B 场新内部模型的能力。四组在劳拉西泮（LZ；一种 GABA A 型受体阳性变构调节剂）、右美沙芬 [DM； N-甲基-D-天冬氨酸 (NMDA) 受体阻断剂]、拉莫三嗪（LG，一种阻断电压门控 Na+ 和 Ca2+ 通道的药物）或东莨菪碱（SP；毒蕈碱受体拮抗剂）。两个对照组在无药物条件下进行测试：一组没有接受额外的实验方案（NP），另一组在第 1 天完成学习和第 2 天开始测试（SD）之间类似 24 小时睡眠剥夺的情况下进行测试。所有组中 A 区域的回忆均正常。 LZ 和 DM 会降低 B 领域的学习能力，但 SP、LG、SD 或 NP 条件下不会降低 B 领域的学习能力。这些结果表明，24 小时睡眠剥夺期可能对这种运动记忆的巩固影响很小或没有影响，并且 NMDA 受体激活和 GABA 能抑制是人类新运动记忆获取但不回忆的机制。
An internal model of the dynamics of a tool or an object is part of the motor memory acquired when learning to use the tool or to manipulate the object. Changes in synaptic efficacy may underlie acquisition and storage of memories. Here we studied the effect of pharmacological agents that interfere with synaptic plasticity on acquisition of new motor memories and on recall of a previously learned internal model. Forty-nine subjects, divided into six groups, made reaching movements while holding a robotic arm that applied forces to the hand. On day 1, all subjects learned to move in force field A. On day 2, each group of subjects was tested on their ability to recall field A and their ability to learn a new internal model in field B. Four groups participated in the experiments of day 2 under the effects of lorazepam (LZ; a GABA type A receptor-positive allosteric modulator), dextromethorphan [DM; an N-methyl-D-aspartate (NMDA) receptor blocker], lamotrigine (LG, a drug that blocks voltage-gated Na+ and Ca2+ channel), or scopolamine (SP; muscarinic receptor antagonist). Two control groups were tested in a drug-free condition: one group that was not exposed to additional experimental protocols (NP) and another group was tested under similar to24 h of sleep deprivation between completion of learning on day 1 and start of testing on day 2 (SD). Recall of field A was normal in all groups. Learning of field B was reduced by LZ and DM but not by SP, LG, SD or in the NP condition. These results suggest that a 24-h sleep-deprivation period may have little or no effect on consolidation of this motor memory and that NMDA receptor activation and GABAergic inhibition are mechanisms operating in the acquisition but not recall of new motor memories in humans.