Detection of capsaicin-evoked release of glutamate from spinal dorsal horn slices of rat with on-line monitoring system
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Cited by (56)
TRPV1 receptor inhibition decreases CCL2-induced hyperalgesia
2014, NeuropharmacologyGroup III metabotropic glutamate receptors and transient receptor potential vanilloid 1 co-localize and interact on nociceptors
2012, NeuroscienceCitation Excerpt :First, basal vesicular cycling (Chavis et al., 1998) and glutamate release (Kumar et al., 2010) have been shown to decrease following activation of group III mGluRs. This could counteract the membrane depolarization caused by TRPV1-induced glutamate release (Ueda et al., 1993; Jin et al., 2009). Second, in a related fashion, this reduced extracellular glutamate may curtail activation of group I mGluRs (Bhave et al., 2001) and ionotropic glutamate receptors (iGluRs) N-methyl-d-aspartate (NMDA) (Du et al., 2003), alpha-amino-3-hydroxy-5-methylisoxazolone-4-propionic acid (AMPA) (Carlton et al., 1995; Coggeshall and Carlton, 1998) and kainate receptors (Du et al., 2006) known to be present on peripheral nociceptors.
Contribution of peripheral vanilloid receptor to the nociception induced by injection of spermine in mice
2011, Pharmacology Biochemistry and BehaviorCitation Excerpt :Thus, we suggest that the peripheral mechanisms involved in spermine-induced nociception are different from the spinal mechanisms. However, the reduction of polyamine-induced nociception by the NMDA antagonists in spinal cord could be indirect since the activation of TRPV1 in spinal cord may release glutamate in vitro (Ueda et al., 1993) and produce an NMDA-mediated nociception in vivo (Okano et al., 1994). However, further studies must be carried out to elucidate the role of spinal TRPV1 in the nociceptive action of intrathecally-injected polyamines.
Involvement of glial cells in the nociceptive behaviors induced by a high-dose of histamine administered intrathecally
2011, European Journal of PharmacologyCitation Excerpt :The nociceptive behaviors induced by 1600 pmol of histamine were dose-dependently suppressed by i.t. pretreatment with either minocycline (0.125–2 nmol) or DL-fluorocitric acid (10–40 pmol), and 2 nmol of minocycline or 40 pmol of DL-fluorocitric acid completely eliminated the histamine-induced nociceptive behaviors (Fig. 1). The single application of a high dose (concentration) of capsaicin causes the depletion of substance P and glutamate in primary afferent nerves, and decreases the release of substance P and glutamate from the primary afferent nerve fibers (Sakurada et al., 1996; Ueda et al., 1993). To assess the involvement of released substance P or glutamate from the primary afferent nerve in the histamine-induced nociceptive behaviors, the effect of a pretreatment with capsaicin (15 nmol, i.t.) on the histamine-induced nociceptive behaviors were determined.
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Present address: Department of Applied Biochemistry, Research Institute for Wakan-yaku, Toyama Medical & Pharmaceutical University, Toyama 930-01, Japan.