Williams C L, Jensen R A
Department of Psychology, Southern Illinois University, Carbondale 62901.
Physiol Behav. 1993 Oct;54(4):659-63. doi: 10.1016/0031-9384(93)90073-o.
When given before or after training, Leu-enkephalin impairs later retention of learning. To replicate these findings, Experiment 1 determined if Leu-enkephalin impairs retention when administered after inhibitory avoidance training. Posttraining injection of 100.0 micrograms/kg of Leu-enkephalin impaired retention relative to saline controls or those receiving a lower dose of this peptide. Since Leu-enkephalin does not cross freely from the blood stream into the brain, this peptide may exert its influence on mnemonic processes by activating peripheral receptors that transmit neural messages to the brain via the vagus nerve. In Experiment 2, 100.0 micrograms/kg Leu-enkephalin impaired retention in unoperated and sham-operated animals although vagotomized animals did not differ significantly from these groups or saline controls. These results suggest that subdiaphragmatic vagotomy may not be sufficient to disrupt the mnemonic effects of Leu-enkephalin. Alternatively, the vagus nerve may be one pathway but not the only pathway by which the activation of peripheral systems may influence the memory storage process.
在训练前或训练后给予亮氨酸脑啡肽，会损害随后的学习记忆能力。为了重复这些研究结果，实验1确定了在抑制性回避训练后给予亮氨酸脑啡肽是否会损害记忆。相对于生理盐水对照组或接受较低剂量该肽的组，训练后注射100.0微克/千克亮氨酸脑啡肽会损害记忆。由于亮氨酸脑啡肽不能自由地从血流进入大脑，这种肽可能通过激活外周受体来影响记忆过程，这些外周受体通过迷走神经向大脑传递神经信息。在实验2中，100.0微克/千克亮氨酸脑啡肽损害了未手术和假手术动物的记忆，尽管迷走神经切断的动物与这些组或生理盐水对照组没有显著差异。这些结果表明，膈下迷走神经切断术可能不足以破坏亮氨酸脑啡肽的记忆效应。或者，迷走神经可能是外周系统激活影响记忆存储过程的一条途径，但不是唯一途径。
