Hassert D L, Miyashita T, Williams C L
Department of Psychology, University of Virginia, Charlottesville, VA 22904-4400, USA.
Behav Neurosci. 2004 Feb;118(1):79-88. doi: 10.1037/0735-7044.118.1.79.
Vagal nerve stimulation (VNS) is known to improve cognitive processing, presumably by affecting activity in central nervous system structures that process recently acquired information. It has long been assumed that these effects are related to stimulation-induced increases of norepinephrine (NE) release in limbic brain structures. The present study examined this hypothesis by administering VNS at an intensity and duration that improves memory and then measuring fluctuations in NE output in the basolateral amygdala (BLA) with in vivo microdialysis. In Experiment 1, VNS caused a 98% increase in NE output relative to baseline. In Experiment 2, methyl atropine was given 10 min before VNS to assess whether stimulation-induced increases in amygdala NE are mediated by afferent or efferent vagal branches. Methyl atropine did not alter NE release in the BLA in comparison with saline. The significance of these findings in understanding how peripheral neural activity modulates limbic structures to encode and store new information into memory is discussed.
已知迷走神经刺激(VNS)可改善认知加工,这可能是通过影响中枢神经系统中处理近期获取信息的结构的活动来实现的。长期以来,人们一直认为这些效应与刺激诱导的边缘脑结构中去甲肾上腺素(NE)释放增加有关。本研究通过以改善记忆的强度和持续时间进行VNS,然后用体内微透析测量基底外侧杏仁核(BLA)中NE输出的波动,来检验这一假设。在实验1中,与基线相比,VNS使NE输出增加了98%。在实验2中,在VNS前10分钟给予甲基阿托品,以评估刺激诱导的杏仁核NE增加是由迷走神经传入支还是传出支介导的。与生理盐水相比,甲基阿托品并未改变BLA中的NE释放。本文讨论了这些发现对于理解外周神经活动如何调节边缘结构以将新信息编码并存储到记忆中的意义。