Effects of focal cortical cooling on somatosensory evoked potentials in rats

Abstract

Although the focal brain cooling technique is widely used to examine brain function, the effects of variations in cortical temperature on sensory information processing and neural mechanisms remain underexplored. To elucidate the mechanisms of temperature modulation in somatosensory processing, this study aimed to examine how P1 and N1 deflections of somatosensory evoked potentials (SEPs) depend on cortical temperature and how excitatory and inhibitory inputs contribute to this temperature dependency. SEPs were generated through electrical stimulation of the contralateral forepaw in anesthetized rats. The SEPs were recorded while cortical temperatures were altered between 18–37°C: without any antagonists; with gamma-aminobutyric acid type A (GABAA) receptor antagonist, gabazine; with aminomethylphosphonic acid (AMPA) receptor antagonist (NBQX), orN-Methyl-D-aspartic acid (NMDA) receptor antagonist ([R]-CPP). The effects of different gabazine concentrations (0, 1, and 10 µM) were examined in the 35–38°C range. The P1/N1 amplitudes and their peak- to-peak differences plotted against cortical temperature showed an inverted U relationship with their maximum at approximately 27.5°C when no antagonists were administered. The negative correlation between these amplitudes and temperatures ≥27.5°C plateaued after gabazine administration, which occurred progressively as the gabazine concentration increased. In contrast, the correlation remained negative after the administration of NBQX and (R)-CPP. GABAergic inhibitory inputs contribute to the negative correlation between SEP amplitude and cortical temperature around the physiological cortical temperature by suppressing SEPs to a greater extent at higher temperatures.