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Clonidine depresses LTP of C-fiber evoked field potentials in spinal dorsal horn via NO-cGMP pathway.
Brain Res. 2006 Nov 06; 1118(1):58-65.BR

Abstract

Clonidine, a specific alpha2-adrenergic receptor agonist, has been found to be effective for the treatment of neuropathic pain, the mechanism underlying the effect is, however, not well understood. Here, the effect of clonidine on long-term potentiation (LTP) of C-fiber evoked field potentials in spinal dorsal horn, which is a synaptic model of injury-induced hyperalgesia, was investigated. LTP of C-fiber evoked field potentials was recorded in the superficial layers of spinal dorsal horn in anesthetized adult Sprague-Dawley rats. Clonidine and other substances were applied locally at the recording spinal segments before or after LTP induction by tetanic stimulation. We found that (1) Clonidine completely blocked LTP induction, when applied 30 min before tetanic stimulation and depressed spinal LTP, when applied 30 min and 3 h after LTP induction. (2) The inhibitory effect of clonidine on spinal LTP had two phases: a fast phase lasting for about 3.5 h and a slow phase persisting for the rest time of experiments (up to 8 h after drug). (3) Spinal clonidine at low dose (10.7 micro g/100 micro l) depressed spinal LTP but not C-fiber baseline response and at higher dose (107 micro g/100 micro l) depressed both of them. (4) Pretreatment with alpha2-adrenergic receptor antagonist yohimbine completely blocked the inhibitory effect of clonidine. (5) Pretreatment with muscarinic receptor antagonist atropine, nitric oxide synthesis inhibitor l-NNA or cGMP inhibitor ODQ depressed the fast phase inhibition significantly and abolished the slow phase inhibition completely. These results suggest that clonidine may exert analgesic effect by depressing the synaptic plasticity in spinal dorsal horn, via activation of muscarinic receptor-NO-cGMP pathway.

Authors+Show Affiliations

Pain Research Center, Department of Physiology, Zhongshan Medical School of Sun Yat-Sen University, Guangzhou, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16950233

Citation

Ge, Yu-Xing, et al. "Clonidine Depresses LTP of C-fiber Evoked Field Potentials in Spinal Dorsal Horn Via NO-cGMP Pathway." Brain Research, vol. 1118, no. 1, 2006, pp. 58-65.
Ge YX, Xin WJ, Hu NW, et al. Clonidine depresses LTP of C-fiber evoked field potentials in spinal dorsal horn via NO-cGMP pathway. Brain Res. 2006;1118(1):58-65.
Ge, Y. X., Xin, W. J., Hu, N. W., Zhang, T., Xu, J. T., & Liu, X. G. (2006). Clonidine depresses LTP of C-fiber evoked field potentials in spinal dorsal horn via NO-cGMP pathway. Brain Research, 1118(1), 58-65.
Ge YX, et al. Clonidine Depresses LTP of C-fiber Evoked Field Potentials in Spinal Dorsal Horn Via NO-cGMP Pathway. Brain Res. 2006 Nov 6;1118(1):58-65. PubMed PMID: 16950233.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Clonidine depresses LTP of C-fiber evoked field potentials in spinal dorsal horn via NO-cGMP pathway. AU - Ge,Yu-Xing, AU - Xin,Wen-Jun, AU - Hu,Neng-Wei, AU - Zhang,Tong, AU - Xu,Ji-Tian, AU - Liu,Xian-Guo, Y1 - 2006/09/01/ PY - 2006/05/26/received PY - 2006/07/29/revised PY - 2006/08/04/accepted PY - 2006/9/5/pubmed PY - 2007/1/24/medline PY - 2006/9/5/entrez SP - 58 EP - 65 JF - Brain research JO - Brain Res. VL - 1118 IS - 1 N2 - Clonidine, a specific alpha2-adrenergic receptor agonist, has been found to be effective for the treatment of neuropathic pain, the mechanism underlying the effect is, however, not well understood. Here, the effect of clonidine on long-term potentiation (LTP) of C-fiber evoked field potentials in spinal dorsal horn, which is a synaptic model of injury-induced hyperalgesia, was investigated. LTP of C-fiber evoked field potentials was recorded in the superficial layers of spinal dorsal horn in anesthetized adult Sprague-Dawley rats. Clonidine and other substances were applied locally at the recording spinal segments before or after LTP induction by tetanic stimulation. We found that (1) Clonidine completely blocked LTP induction, when applied 30 min before tetanic stimulation and depressed spinal LTP, when applied 30 min and 3 h after LTP induction. (2) The inhibitory effect of clonidine on spinal LTP had two phases: a fast phase lasting for about 3.5 h and a slow phase persisting for the rest time of experiments (up to 8 h after drug). (3) Spinal clonidine at low dose (10.7 micro g/100 micro l) depressed spinal LTP but not C-fiber baseline response and at higher dose (107 micro g/100 micro l) depressed both of them. (4) Pretreatment with alpha2-adrenergic receptor antagonist yohimbine completely blocked the inhibitory effect of clonidine. (5) Pretreatment with muscarinic receptor antagonist atropine, nitric oxide synthesis inhibitor l-NNA or cGMP inhibitor ODQ depressed the fast phase inhibition significantly and abolished the slow phase inhibition completely. These results suggest that clonidine may exert analgesic effect by depressing the synaptic plasticity in spinal dorsal horn, via activation of muscarinic receptor-NO-cGMP pathway. SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/16950233/Clonidine_depresses_LTP_of_C_fiber_evoked_field_potentials_in_spinal_dorsal_horn_via_NO_cGMP_pathway_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(06)02365-1 DB - PRIME DP - Unbound Medicine ER -