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Involvement of TRPV4-NO-cGMP-PKG pathways in the development of thermal hyperalgesia following chronic compression of the dorsal root ganglion in rats.
Behav Brain Res. 2010 Mar 17; 208(1):194-201.BB

Abstract

The aim of the present study was to test the hypothesis that the TRPV4-NO-cGMP-PKG cascade is involved in the maintenance of thermal hyperalgesia following chronic compression of the dorsal root ganglion (DRG) (the procedure hereafter termed CCD) in rats. CCD rats showed thermal hyperalgesia and increased nitrite production. Intrathecal administration of ruthenium red (TRPV4 antagonist, 0.1-1 nmol), TRPV4 antisense ODN (TRPV4 AS, 40 microg, daily for 7 days), N(G)-L-nitro-arginine methyl ester (l-NAME, inhibitor of NO synthase, 30-300 nmol), 1H-[1,2,4]-oxadiazolo [4,3-a] quinoxalin-1-one (ODQ, a soluble guanylate cyclase inhibitor, 50-100 nmol) or 8-(4-Chlorophenylthio) guanosine 3',5'-cyclic Monophosphothioate, Rp-Isomer sodium salt (Rp-8-pCPT-cGMPS, a PKG inhibitor, 25-50 nmol) induced a significant (P<0.001) and dose-dependent increase in the paw withdrawal latency (PWL) compared with control rats, respectively. Ruthenium red (1 nmol), TRPV4 AS (40 microg, daily for 7 days) or L-NAME (300 nmol) decreased nitrite (an index of nitric oxide formation) in the DRG of CCD rats. In addition, the phorbol ester 4alpha-phorbol 12,13-didecanoate (4alpha-PDD, TRPV4 synthetic activator, 1 nmol), co-administered with L-NAME (300 nmol), attenuated the suppressive effect of L-NAME on CCD-induced thermal hyperalgesia and nitrite production. Our data suggested that the TRPV4-NO-cGMP-PKG pathway could be involved in CCD-induced thermal hyperalgesia.

Authors+Show Affiliations

Department of Physical Medicine & Rehabilitation, Qilu Hospital, Medical School of Shandong University, Jinan 250012, China.No affiliation info availableNo affiliation info availableNo 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

19948193

Citation

Ding, Xin-Li, et al. "Involvement of TRPV4-NO-cGMP-PKG Pathways in the Development of Thermal Hyperalgesia Following Chronic Compression of the Dorsal Root Ganglion in Rats." Behavioural Brain Research, vol. 208, no. 1, 2010, pp. 194-201.
Ding XL, Wang YH, Ning LP, et al. Involvement of TRPV4-NO-cGMP-PKG pathways in the development of thermal hyperalgesia following chronic compression of the dorsal root ganglion in rats. Behav Brain Res. 2010;208(1):194-201.
Ding, X. L., Wang, Y. H., Ning, L. P., Zhang, Y., Ge, H. Y., Jiang, H., Wang, R., & Yue, S. W. (2010). Involvement of TRPV4-NO-cGMP-PKG pathways in the development of thermal hyperalgesia following chronic compression of the dorsal root ganglion in rats. Behavioural Brain Research, 208(1), 194-201. https://doi.org/10.1016/j.bbr.2009.11.034
Ding XL, et al. Involvement of TRPV4-NO-cGMP-PKG Pathways in the Development of Thermal Hyperalgesia Following Chronic Compression of the Dorsal Root Ganglion in Rats. Behav Brain Res. 2010 Mar 17;208(1):194-201. PubMed PMID: 19948193.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of TRPV4-NO-cGMP-PKG pathways in the development of thermal hyperalgesia following chronic compression of the dorsal root ganglion in rats. AU - Ding,Xin-Li, AU - Wang,Yong-Hui, AU - Ning,Li-Ping, AU - Zhang,Yang, AU - Ge,Hong-You, AU - Jiang,Hong, AU - Wang,Rong, AU - Yue,Shou-Wei, Y1 - 2009/12/03/ PY - 2009/07/25/received PY - 2009/11/18/revised PY - 2009/11/20/accepted PY - 2009/12/2/entrez PY - 2009/12/2/pubmed PY - 2010/5/4/medline SP - 194 EP - 201 JF - Behavioural brain research JO - Behav Brain Res VL - 208 IS - 1 N2 - The aim of the present study was to test the hypothesis that the TRPV4-NO-cGMP-PKG cascade is involved in the maintenance of thermal hyperalgesia following chronic compression of the dorsal root ganglion (DRG) (the procedure hereafter termed CCD) in rats. CCD rats showed thermal hyperalgesia and increased nitrite production. Intrathecal administration of ruthenium red (TRPV4 antagonist, 0.1-1 nmol), TRPV4 antisense ODN (TRPV4 AS, 40 microg, daily for 7 days), N(G)-L-nitro-arginine methyl ester (l-NAME, inhibitor of NO synthase, 30-300 nmol), 1H-[1,2,4]-oxadiazolo [4,3-a] quinoxalin-1-one (ODQ, a soluble guanylate cyclase inhibitor, 50-100 nmol) or 8-(4-Chlorophenylthio) guanosine 3',5'-cyclic Monophosphothioate, Rp-Isomer sodium salt (Rp-8-pCPT-cGMPS, a PKG inhibitor, 25-50 nmol) induced a significant (P<0.001) and dose-dependent increase in the paw withdrawal latency (PWL) compared with control rats, respectively. Ruthenium red (1 nmol), TRPV4 AS (40 microg, daily for 7 days) or L-NAME (300 nmol) decreased nitrite (an index of nitric oxide formation) in the DRG of CCD rats. In addition, the phorbol ester 4alpha-phorbol 12,13-didecanoate (4alpha-PDD, TRPV4 synthetic activator, 1 nmol), co-administered with L-NAME (300 nmol), attenuated the suppressive effect of L-NAME on CCD-induced thermal hyperalgesia and nitrite production. Our data suggested that the TRPV4-NO-cGMP-PKG pathway could be involved in CCD-induced thermal hyperalgesia. SN - 1872-7549 UR - https://www.unboundmedicine.com/medline/citation/19948193/Involvement_of_TRPV4_NO_cGMP_PKG_pathways_in_the_development_of_thermal_hyperalgesia_following_chronic_compression_of_the_dorsal_root_ganglion_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0166-4328(09)00713-X DB - PRIME DP - Unbound Medicine ER -