ArticleThe Journal of physiology2007
Inflammation reduces the contribution of N-type calcium channels to primary afferent synaptic transmission onto NK1 receptor-positive lamina I neurons in the rat dorsal horn.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- An electrophysiologist's guide to dorsal horn excitability and pain.Frontiers in cellular neuroscience · 2025Review
- A novel approach to completely alleviate peripheral neuropathic pain in human patients: insights from preclinical data.Frontiers in neuroanatomy · 2024Review
- CaInternational journal of molecular sciences · 2023Article
- Targeting N-type calcium channels in young-onset of some neurological diseases.Frontiers in cell and developmental biology · 2022Review
- Inflammation induces developmentally regulated sumatriptan inhibition of spinal synaptic transmission.British journal of pharmacology · 2020Article
- Neurokinin-1 Receptor Signaling Is Required for Efficient CaCell reports · 2020Article
- AAV-encoded CaGene therapy · 2019Article
- Impact of gabapentin on neuronal high voltage-activated CaExperimental and therapeutic medicine · 2017Article
- Alternative RNA splicing: contribution to pain and potential therapeutic strategy.Drug discovery today · 2016Review
- Sustained relief of neuropathic pain by AAV-targeted expression of CBD3 peptide in rat dorsal root ganglion.Gene therapy · 2014Article
- Pharmacological Inhibition of Voltage-gated Ca(2+) Channels for Chronic Pain Relief.Current neuropharmacology · 2013Article
- Spinal actions of ω-conotoxins, CVID, MVIIA and related peptides in a rat neuropathic pain model.British journal of pharmacology · 2013Article
- Phorbol ester modulation of Ca2+ channels mediates nociceptive transmission in dorsal horn neurones.Pharmaceuticals (Basel, Switzerland) · 2013Article
- Review
- Ca²⁺-dependent regulation of Ca²⁺ currents in rat primary afferent neurons: role of CaMKII and the effect of injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Presynaptic Cav3.2 channels regulate excitatory neurotransmission in nociceptive dorsal horn neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Opioid-related (ORL1) receptors are enriched in a subpopulation of sensory neurons and prolonged activation produces no functional loss of surface N-type calcium channels.The Journal of physiology · 2012Article
- Regulation of spinal substance p release by intrathecal calcium channel blockade.Anesthesiology · 2011Article
- Subtype-specific reduction of voltage-gated calcium current in medium-sized dorsal root ganglion neurons after painful peripheral nerve injury.Neuroscience · 2011Article
- Inflammatory pain unmasks heterosynaptic facilitation in lamina I neurokinin 1 receptor-expressing neurons in rat spinal cord.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-type calcium channels contribute to the release of glutamate from primary afferent terminals synapsing onto nocisponsive neurons in the dorsal horn of the spinal cord, but little is known of functional adaptations to these channels in persistent pain states. Subtype-selective conotoxins and other drugs were used to determine the role of different calcium channel types in a rat model of inflammatory pain. Electrically evoked primary afferent synapses onto lumber dorsal horn neurons were examined three days after induction of inflammation with intraplantar complete Freund's adjuvant. The maximal inhibitory effect of the N-type calcium channel blockers, omega-conotoxins CVID and MVIIA, were attenuated in NK1 receptor-positive lamina I neurons after inflammation, but the potency of CVID was unchanged. This was associated with reduced inhibition of the frequency of asynchronous-evoked synaptic events by CVID studied in the presence of extracellular strontium, suggesting reduced N-type channel contribution to primary afferent synapses after inflammation. After application of CVID, the relative contributions of P/Q and L channels to primary afferent transmission and the residual current were unchanged by inflammation, suggesting the adaptation was specific to N-type channels. Blocking T-type channels did not affect synaptic amplitude under control or inflamed conditions. Reduction of N-type channel contribution to primary afferent transmission was selective for NK1 receptor-positive neurons identified by post hoc immunohistochemistry and did not occur at synapses in laminae II(o) or II(i), or inhibitory synapses. These results suggest that inflammation selectively downregulates N-type channels in the terminals of primary afferents synapsing onto (presumed) nociceptive lamina I NK1 receptor-positive neurons.
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