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Activation of p38 MAPK in primary afferent neurons by noxious stimulation and its involvement in the development of thermal hyperalgesia.
Pain. 2005 Jan; 113(1-2):51-60.PAIN

Abstract

Alterations in the intracellular signal transduction pathway in primary afferents may contribute to pain hypersensitivity. We demonstrated that very rapid phosphorylation of p38 mitogen-activated protein kinase occurred in dorsal root ganglion (DRG) neurons that were participating in the transmission of noxious signals. Capsaicin injection induced phosphorylated-p38 (p-p38) in small-to-medium diameter sensory neurons with a peak at 2 min after capsaicin injection. Furthermore, we examined the p-p38 labeling in the DRG after noxious thermal stimuli and found a stimulus intensity-dependent increase in labeled cell size and the number of activated neurons. Most of these p-p38-immunoreactive (IR) neurons were small- and medium-sized neurons, which coexpressed transient receptor potential ion channel TRPV1 and phosphorylated-extracellular signal-regulated protein kinase. Intrathecal administration of the p38 inhibitor, FR167653, reversed the thermal hyperalgesia produced by the capsaicin injection. Inhibition of p38 activation was confirmed by the decrease in the number of p-p38-IR neurons in the DRG following capsaicin injection. Taken together, these findings suggest that the activation of p38 pathways in primary afferents by noxious stimulation in vivo may be, at least in part, correlated with functional activity, and further, involved in the development of thermal hyperalgesia.

Authors+Show Affiliations

Department of Anatomy and Neuroscience, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan.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)

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

Language

eng

PubMed ID

15621364

Citation

Mizushima, Toshiyuki, et al. "Activation of P38 MAPK in Primary Afferent Neurons By Noxious Stimulation and Its Involvement in the Development of Thermal Hyperalgesia." Pain, vol. 113, no. 1-2, 2005, pp. 51-60.
Mizushima T, Obata K, Yamanaka H, et al. Activation of p38 MAPK in primary afferent neurons by noxious stimulation and its involvement in the development of thermal hyperalgesia. Pain. 2005;113(1-2):51-60.
Mizushima, T., Obata, K., Yamanaka, H., Dai, Y., Fukuoka, T., Tokunaga, A., Mashimo, T., & Noguchi, K. (2005). Activation of p38 MAPK in primary afferent neurons by noxious stimulation and its involvement in the development of thermal hyperalgesia. Pain, 113(1-2), 51-60.
Mizushima T, et al. Activation of P38 MAPK in Primary Afferent Neurons By Noxious Stimulation and Its Involvement in the Development of Thermal Hyperalgesia. Pain. 2005;113(1-2):51-60. PubMed PMID: 15621364.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Activation of p38 MAPK in primary afferent neurons by noxious stimulation and its involvement in the development of thermal hyperalgesia. AU - Mizushima,Toshiyuki, AU - Obata,Koichi, AU - Yamanaka,Hiroki, AU - Dai,Yi, AU - Fukuoka,Tetsuo, AU - Tokunaga,Atsushi, AU - Mashimo,Takashi, AU - Noguchi,Koichi, PY - 2004/03/16/received PY - 2004/08/27/revised PY - 2004/09/28/accepted PY - 2004/12/29/pubmed PY - 2005/4/19/medline PY - 2004/12/29/entrez SP - 51 EP - 60 JF - Pain JO - Pain VL - 113 IS - 1-2 N2 - Alterations in the intracellular signal transduction pathway in primary afferents may contribute to pain hypersensitivity. We demonstrated that very rapid phosphorylation of p38 mitogen-activated protein kinase occurred in dorsal root ganglion (DRG) neurons that were participating in the transmission of noxious signals. Capsaicin injection induced phosphorylated-p38 (p-p38) in small-to-medium diameter sensory neurons with a peak at 2 min after capsaicin injection. Furthermore, we examined the p-p38 labeling in the DRG after noxious thermal stimuli and found a stimulus intensity-dependent increase in labeled cell size and the number of activated neurons. Most of these p-p38-immunoreactive (IR) neurons were small- and medium-sized neurons, which coexpressed transient receptor potential ion channel TRPV1 and phosphorylated-extracellular signal-regulated protein kinase. Intrathecal administration of the p38 inhibitor, FR167653, reversed the thermal hyperalgesia produced by the capsaicin injection. Inhibition of p38 activation was confirmed by the decrease in the number of p-p38-IR neurons in the DRG following capsaicin injection. Taken together, these findings suggest that the activation of p38 pathways in primary afferents by noxious stimulation in vivo may be, at least in part, correlated with functional activity, and further, involved in the development of thermal hyperalgesia. SN - 0304-3959 UR - https://www.unboundmedicine.com/medline/citation/15621364/Activation_of_p38_MAPK_in_primary_afferent_neurons_by_noxious_stimulation_and_its_involvement_in_the_development_of_thermal_hyperalgesia_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-3959(04)00476-2 DB - PRIME DP - Unbound Medicine ER -