Effect of dexmedetomidine on remifentanil-induced miniature excitatory postsynaptic currents mediated by NMDA receptors in spinal dorsal horn neurons of rats / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the effect of dexmedetomidine on remifentanil-induced miniature excitatory postsynaptic currents (mEPSCs) mediated by N-methyl-D-aspartate (NMDA) receptors in spinal dorsal horn neurons of rats.Methods Thirty male Sprague-Dawley rats,aged 14-18 days,weighing 50-60 g,were used in the study.Their lumbar segments of the spinal cord were immediately removed and sliced.A total of 180 slices were selected and divided into 5 groups (n=36 each) using a random number tableblank control group (group C),remifentanil group (group R),low-dose dexmedetomidine group (group L),moderate-dose dexmedetomidine group (group M) and high-dose dexmedetomidine group (group H).Spinal cord slices were incubated in artificial cerebrospinal fluid (ACSF) for 90 min in group C.Spinal cord slices were incubated for 90 min in ACSF with remifentanil at the final concentration of 4 nmol/L in group R.Spinal cord slices were incubated for 90 min in ACSF with remifentanil at the final concentration of 4 nmol/L and dexmedetomidine at the final concentrations of 2,4 and 6 nmol/L in L,M and H groups,respectively.The whole-cell patch-clamp technique was used to record the amplitude and time interval of NMDA receptors-mediated mEPSCs.Results Compared with group C,the amplitude of mEPSCs was significantly increased,and the time interval of mEPSCs was shortened in the other 4 groups (P＜ 0.05).Compared with group R,the amplitude of mEPSCs was significantly decreased,and the time interval of mEPSCs was prolonged in L,M and H groups (P＜0.05).Compared with group L,the amplitude of mEPSCs was significantly decreased,and the time interval of mEPSCs was prolonged in M and H groups (P＜0.05).Compared with group M,the amplitude of mEPSCs was significantly decreased,and the time interval of mEPSCs was prolonged in group H (P ＜ 0.05).Conclusion Dexmedetomidine weakens remifentanil-induced enhancement in the function of NMDA receptors in spinal dorsal horn neurons probably via the presynaptic and postsynaptie mechanisms in rats.