ArticleMolecular pain2015
In vivo patch-clamp analysis of the antinociceptive actions of TRPA1 activation in the spinal dorsal horn.
Article in Molecular pain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 26 citations in OpenAlex.
- Propofol regulates arousal by enhancing inhibitory synaptic transmission of noradrenergic neurons in the locus coeruleus of adult male mice.Scientific reports · 2025Article
- Disturbed Repolarization-Relaxation Coupling During Acute Myocardial Ischemia Permits Systolic Mechano-Arrhythmogenesis.Circulation research · 2025Article
- Discovery of a potent and selective TRPC3 antagonist with neuroprotective effects.Bioorganic & medicinal chemistry · 2025Article
- Remote neurostimulation through an endogenous ion channel using a near-infrared light-activatable nanoagonist.Science advances · 2024Article
- Transient receptor potential ankyrin 1 in the knee is involved in osteoarthritis pain.Biochemistry and biophysics reports · 2023Article
- Lack of transient receptor potential ankyrin 1 (TRPA1) retards cutaneous wound healing in mice: A preliminary study.Biochemistry and biophysics reports · 2022Article
- Anti-allodynic and promotive effect on inhibitory synaptic transmission of riluzole in rat spinal dorsal horn.Biochemistry and biophysics reports · 2021Article
- Emerging Perspectives on Pain Management by Modulation of TRP Channels and ANO1.International journal of molecular sciences · 2019Review
- Reactive metabolites of acetaminophen activate and sensitize the capsaicin receptor TRPV1.Scientific reports · 2017Article
- TRPA1 channels: molecular sentinels of cellular stress and tissue damage.The Journal of physiology · 2016Review
- Differential Activation of TRP Channels in the Adult Rat Spinal Substantia Gelatinosa by Stereoisomers of Plant-Derived Chemicals.Pharmaceuticals (Basel, Switzerland) · 2016Review
- Emerging Role of Spinal Cord TRPV1 in Pain Exacerbation.Neural plasticity · 2016Review
- Methylglyoxal activates transient receptor potential A1/V1 via reactive oxygen species in the spinal dorsal horn.Molecular painArticle
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTransient receptor potential (TRP) channels are nonselective cation channels expressed in a variety of sensory structures, and are important molecular mediators of thermal, mechanical, cellular and chemical signals. We investigated the function of one key member of the TRP superfamily, TRPA1, in the spinal dorsal horn using in vivo patch-clamp recordings.
resultsThe application of allyl isothiocyanate (AITC), a TRPA1 agonist, significantly increased the frequency and amplitude of inhibitory postsynaptic currents (IPSCs; holding potential (VH) = 0 mV) as well as excitatory postsynaptic currents (EPSCs; VH = -70 mV) in substantia gelatinosa (SG) neurons. The AITC-induced increases in EPSC frequency and amplitude were resistant to the Na(+) channel blocker tetrodotoxin (TTX). In the presence of the glutamate receptor antagonists CNQX and AP5, AITC did not generate any synaptic activity. The AITC-induced increases in IPSC frequency and amplitude were abolished by TTX or glutamate receptor antagonists. Moreover, the duration of IPSCs enhanced by TRPA1 activation were significantly longer than those of EPSCs enhanced by activation of this channel in the spinal dorsal horn. AITC induced hyperpolarization of the membrane potential of SG neurons in the spinal cord but depolarized the membrane potential in the presence of TTX. Furthermore, we examined the effects of mechanical stimuli to the skin during TRPA1 activation in the spinal dorsal horn in normal rats in both voltage-clamp and current-clamp modes. In the peripheral tissue stimuli test, AITC significantly suppressed EPSCs evoked by pinch or air puff stimulation of the skin. In current-clamp mode, AITC significantly suppressed excitatory postsynaptic potentials (EPSPs) evoked by pinch stimuli.
conclusionsTRPA1 appears to be localized not only at presynaptic terminals on SG neurons, enhancing glutamate release, but also in the terminals of primary afferents innervating spinal inhibitory interneurons, which have synaptic interactions with SG neurons. This study offers further insight into the mechanisms underlying the possible antinociceptive actions of TRPA1 activation in the spinal dorsal horn. Our findings suggest that pharmacological activation of spinal TRPA1 channels may have therapeutic potential for the treatment of pain.
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