动物造模 z-bio 2022-03-15 790

　　OBJECTIVE: To study the depolarization rebound and its regulatory mechanism of the colloidal (SG) neurons in the dorsal horn of the spinal cord in rats, in order to provide a reference for the clinical treatment of depolarization rebound related diseases.

　　METHODS: SD rats aged 3-5 weeks were selected to make longitudinal sections of the isolated spinal cord. The electrophysiological characteristics of SG neurons and their response to hyperpolarization stimulation were recorded by whole-cell patch clamp technique, and the hyperpolarization activation loop was observed. Effects of nucleotide-gated cation (HCN) channel blockers and T-type calcium (Cav3) channel blockers on depolarization rebound.

　　RESULTS: The electrical activities of 63 SG neurons were recorded, of which 23 were non-depolarized rebound, 19 were depolarized rebound without discharge, and 21 were depolarized rebound with discharge. The action potential threshold of SG neurons in the non-depolarized rebound group (-28.7±1.6 mV) was significantly higher than that in the depolarized rebound with discharge group (-36.0±2.0 mV) (P<0.05). The HCN channel blockers cesium chloride and ZD7288 significantly prolonged the latency of depolarizing rebound with discharge from 45.9±11.6 ms to 121.6±51.3 ms (P<0.05) and from 36.2±10.3 ms to 73.6±73 ms, respectively (P<0.05). 13.6 ms (P<0.05); ZD7288 also significantly prolonged the latency of depolarized rebound without discharge from 71.9±35.1 ms to 267.0±68.8 ms (P<0.05), while the T-type calcium channel blocker chloride Nickel and mirbedil significantly reduced the amplitude of depolarized rebound concomitant discharge from 19.9±6.3 mV to 9.5±4.5 mV (P<0.05) and from 26.1±9.4 mV to 15.5±5.0 mV (P<0.05), respectively. P<0.05), Mibedil also significantly reduced the amplitude of depolarized rebound without discharge from 14.3±3.0 mV to 7.9±2.0 mV (P<0.05).

　　Conclusion: Nearly 2/3 of SG neurons have depolarization rebound, and their latency and amplitude are regulated by HCN channels and T-type calcium channels, respectively.