Simon Christen, Wallace-Huitt Tiffany, Thapa Priyenka, Skinner Robert D, Garcia-Rill Edgar
Center for Translational Neuroscience, Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences Little Rock, AR, USA.
Front Neurol. 2011 Jan 27;2:3. doi: 10.3389/fneur.2011.00003. eCollection 2011.
The P13 potential is the rodent equivalent of the P50 potential, which is an evoked response recorded at the vertex (Vx) 50 ms following an auditory stimulus in humans. Both the P13 and P50 potentials are only present during waking and rapid eye movement (REM) sleep, and are considered to be measures of level of arousal. The source of the P13 and P50 potentials appears to be the pedunculopontine nucleus (PPN), a brainstem nucleus with indirect ascending projections to the cortex through the intralaminar thalamus, mediating arousal, and descending inhibitory projections to the caudal pontine reticular formation (CPRF), which mediates the auditory startle response (SR). We tested the hypothesis that intracranial microinjection (ICM) of glutamate (GLU) or GLU receptor agonists will increase the activity of PPN neurons, resulting in an increased P13 potential response, and decreased SR due to inhibitory projections from the PPN to the CPRF, in freely moving animals. Cannulae were inserted into the PPN to inject neuroactive agents, screws were inserted into the Vx in order to record the P13 potential, and electrodes inserted into the dorsal nuchal muscle to record electromyograms and SR amplitude. Our results showed that ICM of GLU into the PPN dose-dependently increased the amplitude of the P13 potential and decreased the amplitude of the SR. Similarly, ICM of N-methyl-d-aspartic acid or kainate into the PPN increased the amplitude of the P13 potential. These findings indicate that glutamatergic input to the PPN plays a role in arousal control in vivo, and changes in glutamatergic input, or excitability of PPN neurons, could be implicated in a number of neuropsychiatric disorders with the common symptoms of hyperarousal and REM sleep dysregulation.
P13电位相当于啮齿动物的P50电位，P50电位是人类在听觉刺激后50毫秒在头顶（Vx）记录到的诱发反应。P13和P50电位仅在清醒和快速眼动（REM）睡眠期间出现，被认为是觉醒水平的指标。P13和P50电位的来源似乎是脚桥核（PPN），这是一个脑干核团，通过丘脑板内核向皮层有间接的上行投射，介导觉醒，以及向尾侧脑桥网状结构（CPRF）有下行抑制投射，后者介导听觉惊跳反应（SR）。我们测试了这样一个假设：在自由活动的动物中，向颅内微量注射（ICM）谷氨酸（GLU）或GLU受体激动剂会增加PPN神经元的活性，导致P13电位反应增加，并且由于PPN向CPRF的抑制投射而使SR降低。将套管插入PPN以注射神经活性剂，将螺钉插入Vx以记录P13电位，并将电极插入颈背肌以记录肌电图和SR幅度。我们的结果表明，向PPN内ICM注射GLU会剂量依赖性地增加P13电位的幅度并降低SR的幅度。同样，向PPN内ICM注射N-甲基-D-天冬氨酸或 kainate会增加P13电位的幅度。这些发现表明，PPN的谷氨酸能输入在体内觉醒控制中起作用，并且谷氨酸能输入或PPN神经元兴奋性的变化可能与许多具有高觉醒和REM睡眠失调共同症状的神经精神疾病有关。
