title: [Rebound depolarization of substantia gelatinosa neurons and its modulatory mechanisms in rat spinal dorsal horn].
abstract: OBJECTIVE
  To investigate the rebound depolarization of substantia gelatinosa (SG) neurons in rat spinal dorsal horn and explore its modulatory mechanisms to provide better insights into rebound depolarization-related diseases.
  
  
  METHODS
  Parasagittal slices of the spinal cord were prepared from 3- to 5-week-old Sprague-Dawley rats. The electrophysiologic characteristics and responses to hyperpolarization stimulation were recorded using whole-cell patch-clamp technique. The effects of hyperpolarization-activated cyclic nucleotide gated cation (HCN) channel blockers and T-type calcium channel blockers on rebound depolarization of the neurons were studied.
  
  
  RESULTS
  A total of 63 SG neurons were recorded. Among them, 23 neurons showed no rebound depolarization, 19 neurons showed rebound depolarization without spikes, and 21 neurons showed rebound depolarization with spikes. The action potential thresholds of the neurons without rebound depolarization were significantly higher than those of the neurons with rebound depolarization and spikes (-28.7∓1.6 mV vs -36.0∓2.0 mV, P<0.05). The two HCN channel blockers CsCl and ZD7288 significantly delayed the latency of rebound depolarization with spike 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∓13.6 ms (P<0.05), respectively. ZD7288 also significantly prolonged the latency of rebound depolarization without spike from 71.9∓35.1 ms to 267.0∓68.8 ms (P<0.05). The T-type calcium channel blockers NiCl2 and mibefradil strongly decreased the amplitude of rebound depolarization with spike 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. Mibefradil also significantly decreased the amplitude of rebound depolarization without spike from 14.3∓3.0 mV to 7.9∓2.0 mV (P<0.05).
  
  
  CONCLUSIONS
  Nearly two-thirds of the SG neurons have rebound depolarizations modulated by HCN channel and T-type calcium channel.
authors.affiliation: Department of Pain Clinic, First Affiliated Hospital of Nanchang University, Nanchang, 330006, China. E-mail: 19893395@qq.com.
authors.forename: Ling-Chao
authors.initials: LC
authors.lastname: Li
authors.forename: Da-Ying
authors.initials: DY
authors.lastname: Zhang
authors.forename: Si-Cong
authors.initials: SC
authors.lastname: Peng
authors.forename: Jing
authors.initials: J
authors.lastname: Wu
authors.forename: Chang-Yu
authors.initials: CY
authors.lastname: Jiang
authors.forename: Tao
authors.initials: T
authors.lastname: Liu
mesh_terms: D000200:Action Potentials; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020747:Calcium Channels, T-Type; D016764:Cell Polarity; D002586:Cesium / Q000494:pharmacology; D002712:Chlorides / Q000494:pharmacology; D054815:Cyclic Nucleotide-Gated Cation Channels / Q000037:antagonists & inhibitors; D009474:Neurons / Q000166:cytology*; D018408:Patch-Clamp Techniques; D011743:Pyrimidines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D066148:Spinal Cord Dorsal Horn / Q000166:cytology*; D013376:Substantia Gelatinosa / Q000166:cytology*
chemical_list: D002121:Calcium Channel Blockers; D020747:Calcium Channels, T-Type; D002712:Chlorides; D054815:Cyclic Nucleotide-Gated Cation Channels; D011743:Pyrimidines; C082246:ICI D2788; D002586:Cesium; C028019:cesium chloride