ArticleNeuroscience bulletin2009
Inhibition of P2X receptor-mediated inward current by protein kinase C in small-diameter dorsal root ganglion neurons of adult rats.
Article in Neuroscience bulletin, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Regulation of ATP-gated P2X channels: from redox signaling to interactions with other proteins.Antioxidants & redox signaling · 2014Review
- Activation and regulation of purinergic P2X receptor channels.Pharmacological reviews · 2011Review
- Meeting acute migraine treatment needs through novel treatment formulations.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2010Review
Corrections and comments
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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
objectiveThe aim of the present study is to verify the ATP-induced varied responses in isolated dorsal root ganglion (DRG) neurons of the adult rat, and investigate the modulatory effects of specific P2X receptor agonist beta, gamma-me-ATP and protein kinase C (PKC) on P2X receptor-mediated inward current in DRG neurons.
methodsWhole cell patch-clamp was employed to record the currents on acutely isolated DRG neurons in the adult rats.
resultsbeta, gamma-me-ATP, similar as ATP, evoked 2 distinct subtypes of P2X receptor-mediated inward currents in a dose-dependent manner in DRG neurons. Activation of PKC by phorbol 12, 13-dibutyrate (PDBu) significantly inhibited both subtypes of inward currents mediated by P2X receptors in a dose-dependent manner.
conclusionActivation of PKC negatively modulated the P2X receptor-mediated currents in rat DRG neurons, which may be of benefit to preventing the over-excitation of nociceptor under inflammatory or neuropathic conditions.
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