Abstract
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.
Highlights
The P50 potential is a midlatency auditory evoked response recorded at the vertex (Vx) and occurs approximately 40–70 ms following an auditory click stimulus (Picton et al, 1974)
Intracranial microinjection (ICM) of N-methyl-d-aspartic acid or kainate into the pedunculopontine nucleus (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 rapid eye movement (REM) sleep dysregulation
Major findings include (1) ICM of GLU into the PPN of the rat dose-dependently increased the amplitude of the P13 potential and decreased startle response (SR) amplitude, and (2) ICM of the specific agonists N-methyl-d-aspartic acid (NMDA) and KA increased the amplitude of the P13 potential, which was blocked by pretreatment with the respective receptor antagonists
Summary
The P50 potential is a midlatency auditory evoked response recorded at the vertex (Vx) and occurs approximately 40–70 ms following an auditory click stimulus (Picton et al, 1974). The P13 potential in the freely moving rat occurs 11–15 ms following a click stimulus, is only present during waking and REM sleep, is blocked by scopolamine (Miyazato et al, 1995), and appears to be the rodent equivalent to the human P50 potential (Miyazato et al, 1995, 1996, 1999a,c; Teneud et al, 2000). Both the P13 and P50 potentials are considered to be measures of level of arousal (Garcia-Rill et al, 2002). Decreasing arousal levels through the use of anesthetics, ethanol, or head injury decreased the amplitude of the P13 potential (Miyazato et al, 1999a)
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