ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2011
Activation of CaMKII and ERK1/2 contributes to the time-dependent potentiation of Ca2+ response elicited by repeated application of capsaicin in rat DRG neurons.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 32 citations in OpenAlex.
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- TRPV1 channels contribute to spontaneous glutamate release in nucleus tractus solitarii following chronic intermittent hypoxia.Journal of neurophysiology · 2019Article
- Capsaicin induces browning of white adipose tissue and counters obesity by activating TRPV1 channel-dependent mechanisms.British journal of pharmacology · 2016Article
- Paeoniflorin protects diabetic mice against myocardial ischemic injury via the transient receptor potential vanilloid 1/calcitonin gene-related peptide pathway.Cell & bioscience · 2016Article
- Activation of TRPC channels contributes to OA-NO2-induced responses in guinea-pig dorsal root ganglion neurons.The Journal of physiology · 2014Article
- Nitro-oleic acid desensitizes TRPA1 and TRPV1 agonist responses in adult rat DRG neurons.Experimental neurology · 2014Article
- Capsaicin-induced activation of ERK1/2 and its involvement in GAP-43 expression and CGRP depletion in organotypically cultured DRG neurons.Cellular and molecular neurobiology · 2013Article
- Permeation and block of TRPV1 channels by the cationic lidocaine derivative QX-314.Journal of neurophysiology · 2013Article
- P2X₃ and TRPV1 functionally interact and mediate sensitization of trigeminal sensory neurons.Neuroscience · 2013Article
- Activation of neurokinin-1 receptors increases the excitability of guinea pig dorsal root ganglion cells.The Journal of pharmacology and experimental therapeutics · 2012Article
- Tipping the balance of autism risk: potential mechanisms linking pesticides and autism.Environmental health perspectives · 2012Article
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3 authors at 1 institution in 1 country.
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Abstract
When capsaicin is applied repeatedly to dorsal root ganglion (DRG) neurons for brief periods (10-15 s) at short intervals (5-10 min), the evoked responses rapidly decline, a phenomenon termed tachyphylaxis. In addition to this phenomenon, the present study using Ca(2+) imaging revealed that repeated application of capsaicin to rat dissociated DRG neurons at longer intervals (20-40 min) or during multiple applications at short intervals elicited an enhancement of the responses, termed potentiation. The potentiation occurred in 50-60% of the capsaicin-responsive cells, on average representing a 20- to 30% increase in the peak amplitude of the Ca(2+) signal, and was maximal at a 40-min application interval. An analysis of the mechanisms underlying potentiation revealed that it was suppressed by block of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) with 5 μM KN-93 or block of the activation of extracellular signal-regulated kinase (ERK) 1/2 with 2 μM U-0126. Lowering the extracellular Ca(2+) concentration from 2 to 1 mM or pretreatment with deltamethrin (1 μM), which blocks calcineurin and tachyphylaxis, enhanced potentiation. Potentiation was not affected by: 1) inhibition of protein kinase C or protein kinase A, 2) block of the three subtypes of neurokinin receptors, or 3) block of the trafficking of transient receptor potential V1 channel to the membrane. These results indicate that the potentiation is a slowly developing Ca(2+)-modulated process that is mediated by a complex intracellular signaling pathway involving activation of CaMKII and ERK1/2. Potentiation may be an important peripheral autosensitization mechanism that occurs independently of the pronociceptive effects of inflammatory mediators and neurotrophic factors.
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