Evidence map›Paper›PMID 28219864›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2016

[Rebound depolarization of substantia gelatinosa neurons and its modulatory mechanisms in rat spinal dorsal horn].

Ling-Chao Li, Da-Ying Zhang, Si-Cong Peng, Jing Wu, Chang-Yu Jiang, Tao Liu

Abstract read
In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Ling-Chao LiDepartment of Pain Clinic, First Affiliated Hospital of Nanchang University, Nanchang, 330006, China. E-mail: 19893395@qq.com.
Da-Ying Zhang
Si-Cong Peng
Jing Wu
Chang-Yu Jiang
Tao Liu
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo 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.

methodsParasagittal 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.

resultsA 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).

conclusionNearly two-thirds of the SG neurons have rebound depolarizations modulated by HCN channel and T-type calcium channel.

Indexed as

Action PotentialsAnimalsCalcium Channel BlockersCalcium Channels, T-TypeCell PolarityCesiumChloridesCyclic Nucleotide-Gated Cation ChannelsNeuronsPatch-Clamp TechniquesPyrimidinesRatsRats, Sprague-DawleySpinal Cord Dorsal HornSubstantia GelatinosaCalcium Channel BlockersCalcium Channels, T-TypeCesiumcesium chlorideChloridesCyclic Nucleotide-Gated Cation ChannelsICI D2788Pyrimidines

Identifiers

PMID28219864
PMCPMC6779672
OpenAlexW3024798237

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.