Effect of ketamine on sensory processing of thalamocortical circuits in rats / 中华麻醉学杂志

ABSTRACT

Objective To investigate the effect of ketamine injected into the ventral posteromedial nucleus (VPM) of the thalamus on sensory processing of thalamocortical circuits in rats.Methods Twenty-four SpragueDawley rats in which the neurophysiological model was successfully established,aged 2 months,weighing 280-350g,were randomly divided into 4 groups (n=6 each)control group (group C),specific inhibitor of NMDA receptors AP-5 group (group A) and two different concentrations of ketamine groups (K1 and K2 groups).Normal saline 1 μl,AP-5 5 μg/μl and ketamine 12.5 and 25.0 μg/μl were injected into the VPM in A,AP-5,K1 and K2groups,respectively.Somatosensory-evoked potentials (SEPs) in the primary somatosensory cortex (S1) of the rat was recoded at 4 time periods300 s before administration-immediately after administration (baseline,T0),immediately after administration-300 s after administration (T1),300-600 s after administration (T2),600-900 s after administration (T3).Results Compared with the baseline value at T0,there was no significant difference in the peak amplitude of SEPs at T1-3 in group C (P ＞ 0.05),and the peak amplitude of SEPs was significantly decreased at T1-3 in A,K1 and K2 groups (P ＜ 0.05).Compared with group C,the peak amplitude of SEPs was significantly decreased at T1-3 in A,K1 and K2 groups (P ＜ 0.05).Compared with group A,the peak amplitude of SEPs was significantly increased at T3 in group K1 (P ＜ 0.05).There was no significant difference in the peak amplitude of SEPs between A and K2 groups,K1 and K2 groups (P ＞ 0.05).Conclusion Ketamine results in damage to the integrity of sensory processing of thalamocortical circuits and reduction of incoming sensory information,and the mechanism may be related to blockade of NMDA receptors in VPM of the thalamus.