ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Inhibition of N-type voltage-activated calcium channels in rat dorsal root ganglion neurons by P2Y receptors is a possible mechanism of ADP-induced analgesia.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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54 citing papers in PubMed, 124 citations in OpenAlex.
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- Interleukin-1α links peripheral CaScientific reports · 2024Article
- Insights on Platelet-Derived Growth Factor Receptor α-Positive Interstitial Cells in the Male Reproductive Tract.International journal of molecular sciences · 2024Review
- Interleukin-1α links peripheral CabioRxiv : the preprint server for biology · 2024Article
- P2Y1 Receptor as a Catalyst of Brain Neurodegeneration.NeuroSci · 2022Review
- Purinergic receptor antagonism: A viable strategy for the management of autonomic dysreflexia?Autonomic neuroscience : basic & clinical · 2021Article
- Neuropathic Pain in Multiple Sclerosis and Its Animal Models: Focus on Mechanisms, Knowledge Gaps and Future Directions.Frontiers in neurology · 2021Review
- Deletion of the Gene Encoding the NMDA Receptor GluN1 Subunit in Schwann Cells Causes Ultrastructural Changes in Remak Bundles and Hypersensitivity in Pain Processing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Purinergic signaling as a basis of acupuncture-induced analgesia.Purinergic signalling · 2020Review
- Nociceptor Signalling through ion Channel Regulation via GPCRs.International journal of molecular sciences · 2019Review
- Glutamate-induced and NMDA receptor-mediated neurodegeneration entails P2Y1 receptor activation.Cell death & disease · 2018Article
- The Metabotropic Purinergic P2Y Receptor Family as Novel Drug Target in Epilepsy.Frontiers in pharmacology · 2018Review
- Evidence of activity-dependent plasticity in the dorsal cochlear nucleus, in vivo, induced by brief sound exposure.Hearing research · 2016Article
- Membrane coordination of receptors and channels mediating the inhibition of neuronal ion currents by ADP.Purinergic signalling · 2016Article
- Signaling mechanism for modulation by ATP of glycine receptors on rat retinal ganglion cells.Scientific reports · 2016Article
- Phosphoinositide signaling in somatosensory neurons.Advances in biological regulation · 2016Review
- P2Y Receptors in Synaptic Transmission and Plasticity: Therapeutic Potential in Cognitive Dysfunction.Neural plasticity · 2016Review
- Chronic inflammatory pain upregulates expression of P2Y2 receptor in small-diameter sensory neurons.Metabolic brain disease · 2015Article
- [Pharmacological aspects of pain research in Germany].Schmerz (Berlin, Germany) · 2015Review
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patch-clamp recordings from small-diameter rat dorsal root ganglion (DRG) neurons maintained in culture demonstrated preferential inhibition by ATP of high-voltage-activated, but not low-voltage-activated, Ca2+ currents (I(Ca)). The rank order of agonist potency was UTP > ADP > ATP. ATP depressed the omega-conotoxin GVIA-sensitive N-type current only. Pyridoxal-5-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) and 2'-deoxy-N6-methyladenosine 3',5'-bisphosphate tetraammonium, two P2Y1 receptor antagonists, almost abolished the ATP-induced inhibition. Both patch-clamp recordings and immunocytochemistry coupled with confocal laser microscopy indicated a colocalization of functional P2X3 and P2Y1 receptors on the same DRG neurons. Because the effect of ATP was inhibited by intracellular guanosine 5'-O-(2-thiodiphosphate) or by applying a strongly depolarizing prepulse, P2Y1 receptors appear to block I(Ca) by a pathway involving the betagamma subunit of a G(q/11) protein. Less efficient buffering of the intracellular Ca2+ concentration ([Ca2+]i) by reducing the intrapipette EGTA failed to interfere with the ATP effect. Fura-2 microfluorimetry suggested that ATP raised [Ca2+]i by a Galpha-mediated release from intracellular pools and simultaneously depressed the high external potassium concentration-induced increase of [Ca2+]i by inhibiting I(Ca) via Gbetagamma. Adenosine 5'-O-(2-thiodiphosphate) inhibited dorsal root-evoked polysynaptic population EPSPs in the hemisected rat spinal cord and prolonged the nociceptive threshold on intrathecal application in the tail-flick assay. These effects were not antagonized by PPADS. Hence, P2Y receptor activation by ADP, which is generated by enzymatic degradation of ATP, may decrease the release of glutamate from DRG terminals in the spinal cord and thereby partly counterbalance the algogenic effect of ATP.
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