Posttraining electrical stimulation of vagal afferents with concomitant vagal efferent inactivation enhances memory storage processes in the rat
Posttraining electrical stimulation of vagal afferents with concomitant vagal efferent inactivation enhances memory storage processes in the rat
复制标题
DOI：
10.1006/nlme.1998.3863
复制
发表时间：
1998-11-01
影响因子：
2.7
通讯作者：
Jensen, RA
中科院分区：
文献类型：
--
作者：
Clark, KB;Smith, DC;Jensen, RA
外周给药或释放的物质调节记忆存储，但不能自由进入大脑，可能通过激活通过迷走神经集中发送信息的外周受体来对记忆产生影响。的确，迷走神经刺激增强了记忆能力，尽管目前尚不清楚这种效果是由于迷走神经传入或传出的激活所致。为了消除下行纤维对记忆存储过程的可能影响，大鼠在左侧颈迷走神经旁植入袖带电极/导管系统。术后48h，每只动物在刺激点下方注入3.0mU的L液(1.0mU L/分钟)或75.0mM的利多卡因或等渗盐水。10分钟后，动物接受0.75mA、1.0mA S足电击进行抑制-回避任务训练。训练结束后立即给予假刺激或迷走神经刺激(0.5ms双相脉冲；20.0 Hz；30 S；0.2、0.4或0.8 mA)。24 h后，通过刺激迷走神经下行纤维灭活或不灭活来增强记忆。利多卡因组和生理盐水组均表现出强度依赖的倒U形固位模式，0.4 mA时效果最好(U=9，p<；0.05，U=7，p<；0.01)。此外，与注射生理盐水的对照组相比，接受利多卡因注射但没有迷走神经刺激的动物表现出记忆障碍(U=11，p<；0.05)。总之，这些发现表明，迷走神经传入携带有关外周状态的信息，导致记忆存储的调节，迷走神经刺激产生的记忆增强效应并不是通过激活迷走神经传出而介导的。(C)1998年学术出版社。
Peripherally administered or released substances that modulate memory storage, but do not freely enter the brain, may produce their effects on memory by activating peripheral receptors that send messages centrally through the vagus nerve. Indeed, vagus nerve stimulation enhances memory performance, although it is unclear whether this effect is due to the activation of vagal afferents or efferents. To eliminate the possible influence of descending fibers on memory storage processes, rats were implanted with cuff electrode/catheter systems along the left cervical vagus. Forty-eight hours following surgery, each animal received a 3.0-mu l infusion (1.0 mu l/min) of either lidocaine hydrochloride (75.0 mM) or isotonic saline below the point of stimulation. Animals were then trained 10 min later on an inhibitory-avoidance task with a 0.75-mA, 1.0-s foot shock. Sham stimulation or vagus nerve stimulation (0.5-ms biphasic pulses; 20.0 Hz; 30 s; 0.2, 0.4, or 0.8 mA) was administered immediately after training. Memory, tested 24 h later, was enhanced by stimulation whether descending vagus nerve fibers were inactivated or not. Both lidocaine- and saline-infused groups showed an intensity-dependent inverted-U-shaped pattern of retention performance, with the greatest effect observed for 0.4 mA (U = 9, p < .05, and U = 7, p < .01, respectively). Additionally, animals that received lidocaine infusions, but no vagus nerve stimulation, showed impaired memory compared to the performance of saline-infused control animals (U = 11, p < .05). Together, these findings suggest that vagal afferents carry messages about peripheral states that lead to the modulation of memory storage and that the memory-enhancing effect produced by vagus nerve stimulation is not mediated via the activation of vagal efferents. (C) 1998 Academic Press.