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Different roles of spinal p38 and c-Jun N-terminal kinase pathways in bee venom-induced multiple pain-related behaviors.
Neurosci Lett. 2007 Oct 29; 427(1):50-4.NL

Abstract

Our previous studies have established the idea that different types of pain induced by subcutaneous bee venom (BV) injection might be mediated by different spinal signaling pathways. To further testify this hypothesis, the present investigation was designed to detect whether spinal p38 and c-Jun N-terminal kinase (JNK) pathways are equally or differentially involved in the development of persistent spontaneous nociception (PSN), primary heat and mechanical hyperalgesia, and mirror-image heat (MIH) hypersensitivity in the BV model, by evaluating the effects of intrathecal (i.t.) pre-administration of a p38 inhibitor SB239063 and a JNK inhibitor SP600125 in the conscious rat. The results showed that i.t. pre-treatment with either SB239063 or SP600125 caused a significant prevention of BV-induced persistent paw flinching reflex in a dose-related manner, with the former exhibiting much stronger inhibition than the latter. Moreover, the same doses of SB239063 and SP600125 also exhibited different suppressive actions on the induction of primary heat hyperalgesia and MIH hypersensitivity. That is, SP600125 produced a larger increase of thermal latency than SB239063 in the injected paw, whereas SB239063 mainly affected the value measured in the non-injected paw. Pre-treatment with neither SB239063 nor SP600125 had any effect on BV-evoked mechanical hyperalgesia. Taken together, these data suggest that activation of p38 in the spinal cord preferentially contributes to the development of PSN and MIH hypersensitivity under pathological state, while spinal JNK signaling pathways might play more important roles in inducing primary heat hyperalgesia.

Authors+Show Affiliations

Institute for Biomedical Sciences of Pain and Institute for Functional Brain Disorders, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, 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

17923327

Citation

Cao, Fa-Le, et al. "Different Roles of Spinal P38 and c-Jun N-terminal Kinase Pathways in Bee Venom-induced Multiple Pain-related Behaviors." Neuroscience Letters, vol. 427, no. 1, 2007, pp. 50-4.
Cao FL, Liu MG, Hao J, et al. Different roles of spinal p38 and c-Jun N-terminal kinase pathways in bee venom-induced multiple pain-related behaviors. Neurosci Lett. 2007;427(1):50-4.
Cao, F. L., Liu, M. G., Hao, J., Li, Z., Lu, Z. M., & Chen, J. (2007). Different roles of spinal p38 and c-Jun N-terminal kinase pathways in bee venom-induced multiple pain-related behaviors. Neuroscience Letters, 427(1), 50-4.
Cao FL, et al. Different Roles of Spinal P38 and c-Jun N-terminal Kinase Pathways in Bee Venom-induced Multiple Pain-related Behaviors. Neurosci Lett. 2007 Oct 29;427(1):50-4. PubMed PMID: 17923327.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Different roles of spinal p38 and c-Jun N-terminal kinase pathways in bee venom-induced multiple pain-related behaviors. AU - Cao,Fa-Le, AU - Liu,Ming-Gang, AU - Hao,Jian, AU - Li,Zhen, AU - Lu,Zhuo-Min, AU - Chen,Jun, Y1 - 2007/09/08/ PY - 2007/07/27/received PY - 2007/08/24/revised PY - 2007/09/05/accepted PY - 2007/10/10/pubmed PY - 2008/1/26/medline PY - 2007/10/10/entrez SP - 50 EP - 4 JF - Neuroscience letters JO - Neurosci Lett VL - 427 IS - 1 N2 - Our previous studies have established the idea that different types of pain induced by subcutaneous bee venom (BV) injection might be mediated by different spinal signaling pathways. To further testify this hypothesis, the present investigation was designed to detect whether spinal p38 and c-Jun N-terminal kinase (JNK) pathways are equally or differentially involved in the development of persistent spontaneous nociception (PSN), primary heat and mechanical hyperalgesia, and mirror-image heat (MIH) hypersensitivity in the BV model, by evaluating the effects of intrathecal (i.t.) pre-administration of a p38 inhibitor SB239063 and a JNK inhibitor SP600125 in the conscious rat. The results showed that i.t. pre-treatment with either SB239063 or SP600125 caused a significant prevention of BV-induced persistent paw flinching reflex in a dose-related manner, with the former exhibiting much stronger inhibition than the latter. Moreover, the same doses of SB239063 and SP600125 also exhibited different suppressive actions on the induction of primary heat hyperalgesia and MIH hypersensitivity. That is, SP600125 produced a larger increase of thermal latency than SB239063 in the injected paw, whereas SB239063 mainly affected the value measured in the non-injected paw. Pre-treatment with neither SB239063 nor SP600125 had any effect on BV-evoked mechanical hyperalgesia. Taken together, these data suggest that activation of p38 in the spinal cord preferentially contributes to the development of PSN and MIH hypersensitivity under pathological state, while spinal JNK signaling pathways might play more important roles in inducing primary heat hyperalgesia. SN - 0304-3940 UR - https://www.unboundmedicine.com/medline/citation/17923327/Different_roles_of_spinal_p38_and_c_Jun_N_terminal_kinase_pathways_in_bee_venom_induced_multiple_pain_related_behaviors_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-3940(07)00964-0 DB - PRIME DP - Unbound Medicine ER -