Distribution of TRPV1 in CSF Contacting Nucleus of Rat Brain Parenchyma and its expression in Neuropathic PainChun- Xu1, Zi-jun Zhao1, Ting-ting Wu1 and Li-cai Zhang2*
- Corresponding Author:
- Dr. Li-Cai Zhang
Jiangsu Province Key Laboratory of Anesthesiology
Xuzhou Medical College, Xuzhou 221002, PR China.
Tel: 86- 516-85748431
E-mail: [email protected]
Received date: May 12, 2011; Accepted date: July 13, 2011; Published date: July 15, 2011
Citation: Xu C, Zhao Z, Wu T, Zhang L (2011) Distribution of TRPV1 in CSF Contacting Nucleus of Rat Brain Parenchyma and its expression in Neuropathic Pain. J Neurol Neurophysiol 2:114. doi:10.4172/2155-9562.1000114
Copyright: © 2011 Xu C, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: The cerebrospinal fluid-contacting nucleus (CSF-CN), distributes and localizes in the ventral periaqueductal central gray (PAG) of the brainstem, which may influence actual composition of the cerebrospinal fluid (CSF) for non-synaptic signal transmission via releasing or absorbing bioactive substance. TRPV1 has been found in both the peripheral and spinal within centres known for their role in pain detection, transmission and regulation, consistent with its role in pain. Therefore, it is speculated that the CSF-CN participate in pain modulation via the receptor TRPV1. The present study aimed to observe the TRPV1 expression and distribution in the CSF-CN of rat brain parenchyma, and to explore the effects of TRPV1 on the CSF-CN in neuropathic pain.
Methods: The model of neuropathic pain with chronic constriction injury (CCI) of the sciatic nerve was made in Spague-Dawley rats. The thermal withdrawal latency (TWL) and mechanical withdrawal threshold (MWT) were measured. The cholera toxin subunit B conjugated with horseradish peroxidase (CB-HRP) as a tracer was injected into one of the rats’ lateral ventricles (LV) to explore CSF-CN. The distribution and expression of TRPV1 were observed in the CSF-CN with double labeling of CB-HRP and TRPV1 with immunhistochemistry. A selective TRPV1 antagonist, SB-366791, was injected into one of the rat’s LV at the day of peak raise of allodynia and hyperalgesia (10 days after CCI surgery) in 5μg. The behavioral of rat were observed at 2h before and 0.5,1, 2, 4, and 8h after administration.
Results: The CSF-CN is always located in a special region in rat brain parenchyma which is well consistent with the previous finding and found that most cells of CSF-CN have TRPV1. TRPV1 expression levels were significantly increased in the CB-HRP positive neurons at 10 days following CCI surgery. After intracerebroventricular administration of SB366791, mechanical allodynia and thermal hyperalgesia were attenuated at 5μg over a time period of approximately 4 hours, especially at 2h following administration.
Conclusions: TRPV1 is localized within the CSF-CN of the mesencephalon and its expression was increased in CSF-CN by CCI surgery. Comparative analgesic effects of a TRPV1 anatagonist in a CCI model of neuropathic pain lend support to the validation of TRPV1 in CSF-CN as a promising target for the treatment of neuropathic pain.