use-vivo-single-fiber-recording-intact-dorsal-root-ganglion-with

Use of In Vivo Single-fiber Recording and Intact Dorsal Root Ganglion with Attached Sciatic Nerve to Examine the Mechanism of Conduction Failure

Single-fiber recording has been a classical and effective electrophysiological technique over the last few decades because of its specific application for ...

Peking University

To observe the change in induction of long-term potentiation (LTP) of C-fiberevoked potentials in the spinal dorsal horn of neuropathic pain rats, examine the changes in plasticity of synaptic transmission, and explore the effects and mechanisms of central sensitization and neuropathic pain following noxious stimulation or nerve injury.

[Changes in long-term synaptic plasticity in the spinal dorsal horn of neuropathic pain rats].

To observe the effect of 2 Hz electroacupuncture (EA) on long-term depression (LTD) of synaptic transmission in the spinal dorsal horn in rats with neuropathic pain, so as to explore the central mechanisms of the antinociceptive effects of 2 Hz electroacupuncture on neuropathic pain.

[Electroacupuncture of 2 Hz induces long-term depression of synaptic transmission in the spinal dorsal horn in rats with neuropathic pain].

There is current interest in understanding the molecular mechanisms of tumor-induced bone pain. Accumulated evidence shows that endogenous formaldehyde concentrations are elevated in the blood or urine of patients with breast, prostate or bladder cancer. These cancers are frequently associated with cancer pain especially after bone metastasis. It is well known that transient receptor potential vanilloid receptor 1 (TRPV1) participates in cancer pain. The present study aims to demonstrate that the tumor tissue-derived endogenous formaldehyde induces bone cancer pain via TRPV1 activation under tumor acidic environment.

Tumor tissue-derived formaldehyde and acidic microenvironment synergistically induce bone cancer pain.

Besides the injured peripheral dorsal root ganglion (DRG) neurons, the adjacent intact DRG neurons also have important roles in neuropathic pain. Ion channels including Ca3.2 T-type calcium channel in the DRG neurons are important in the development of neuropathic pain. In the present study, we aimed to examine the expression of Ca3.2 T-type calcium channels in the intact DRG neurons in neuropathic pain. A neuropathic pain model of rat with lumbar 5 (L5) spinal nerve ligation (SNL) was established, in which the L4 DRG was separated from the axotomized L5 DRG, and the molecular, morphological and electrophysiological changes of Ca3.2 T-type calcium channels in L4 DRG neurons were investigated. Western blotting showed that total and membrane protein levels of Ca3.2 in L4 DRG neurons increased, and voltage-dependent patch clamp recordings revealed an increased T-type current density with a curve shift to the left in steady-state activation in the acutely isolated L4 DRG neurons in neuropathic pain rats. Immunofluorescent staining further showed that the membrane expression of Ca3.2 increased in CGRP-, IB4-positive small neurons and NF200-positive large ones. In conclusion, the membrane expression and the function of Ca3.2 T-type calcium channels are increased in the intact L4 DRG neurons in neuropathic pain rats with peripheral nerve injury like SNL.

Upregulation of Ca3.2 T-type calcium channels in adjacent intact L4 dorsal root ganglion neurons in neuropathic pain rats with L5 spinal nerve ligation.

The T-type calcium channels Ca3.2, one of the low voltage-activated (LVA) calcium channels, have been found to play important roles in the neuronal excitability. Recently, we and others have demonstrated that accumulation of Ca3.2 channels in the dorsal root ganglion (DRG) neurons and sensory nerves contributes to neuropathic pain after peripheral nerve injury. In the present study, we aimed to further investigate the regulation of Ca3.2 channels by interleukin-6 (IL-6) in DRG neurons in neuropathic pain rats after spinal nerve ligation (SNL). The results showed that Ca3.2 channel protein expression in L5 DRG neurons was upregulated and blockade of this channel decreased the hyperexcitability of DRG neurons and mechanical allodynia in SNL neuropathic pain rats. Furthermore, inhibition of IL-6 trans-signaling reduced the upregulation of Ca3.2 T-type channel induced by FIL-6 (a fusion protein of IL-6 and sIL-6R) in primary cultured DRG neurons in vitro. In vivo, inhibition of IL-6 trans-signaling reversed the upregulation of Ca3.2, reduced the hyperexcitability of L5 DRG neurons and alleviated mechanical allodynia in SNL rats. Our results suggest that IL-6 upregulates Ca3.2 T-type channels expression and function through the IL-6/sIL-6R trans-signaling pathway in DRG neurons, thus contributes to the development of neuropathic pain in SNL rats.

Upregulation of interleukin-6 on Ca3.2 T-type calcium channels in dorsal root ganglion neurons contributes to neuropathic pain in rats with spinal nerve ligation.

FengYu Liu

Neuroscience Research Institute,
Key Lab for Neuroscience,
Ministry of Education/National Health Commission,
Neuroscience Research Institute, Key Lab for Neuroscience, Ministry of Education/National Health Commission

Peking University

Use of In Vivo Single-fiber Recording and Intact Dorsal Root Ganglion with Attached Sciatic Nerve to Examine the Mechanism of Conduction Failure

FengYu Liu

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Neuroscience Research Institute,Key Lab for Neuroscience,Ministry of Education/National Health Commission,Neuroscience Research Institute, Key Lab for Neuroscience, Ministry of Education/National Health Commission

Peking University

Use of In Vivo Single-fiber Recording and Intact Dorsal Root Ganglion with Attached Sciatic Nerve to Examine the Mechanism of Conduction Failure

Neuroscience Research Institute,
Key Lab for Neuroscience,
Ministry of Education/National Health Commission,
Neuroscience Research Institute, Key Lab for Neuroscience, Ministry of Education/National Health Commission