Propofol Modulates Agonist-induced Transient Receptor Potential Vanilloid Subtype-1 Receptor Desensitization via a Protein Kinase Cϵ-dependent Pathway in Mouse Dorsal Root Ganglion Sensory Neurons

@article{Wickley2010PropofolMA,
  title={Propofol Modulates Agonist-induced Transient Receptor Potential Vanilloid Subtype-1 Receptor Desensitization via a Protein Kinase Cϵ-dependent Pathway in Mouse Dorsal Root Ganglion Sensory Neurons},
  author={Peter J. Wickley and Ryo Yuge and Mary S. Russell and Hongyu Zhang and Michael Sulak and Derek S Damron},
  journal={Anesthesiology},
  year={2010},
  volume={113},
  pages={833-844}
}
Background:The activity of transient receptor potential vanilloid subtype-1 (TRPV1) receptors, key nociceptive transducers in dorsal root ganglion sensory neurons, is enhanced by protein kinase C ϵ (PKCϵ) activation. The intravenous anesthetic propofol has been shown to activate PKCϵ. Our objectives were to examine whether propofol modulates TRPV1 function in dorsal root ganglion neurons via activation of PKCϵ. Methods:Lumbar dorsal root ganglion neurons from wild-type and PKCϵ-null mice were… 

Propofol restores transient receptor potential vanilloid receptor subtype-1 sensitivity via activation of transient receptor potential ankyrin receptor subtype-1 in sensory neurons.

It is demonstrated that propofol restores TRPV1 sensitivity in primary DRG neurons and in cultured F-11 cells transfected with both the TRpV1 and TRPA1 receptors via aTRPA1-dependent process.

Propofol restores TRPV1 sensitivity via a TRPA1-, nitric oxide synthase-dependent activation of PKCε

The data indicate that the AITC‐ and propofol‐induced restoration of TRPV1 sensitivity is mediated by a TRPA1‐dependent, nitric oxide synthase‐dependent activation of PKCε.

Orexin A Inhibits Propofol-Induced Neurite Retraction by a Phospholipase D / Protein Kinase C-epsilon-Dependent Mechanism in Neurons

OA blocks propofol-induced neurite retraction by a PLD/PKCe-mediated pathway, and PKCe maybe the key enzyme where the wakefulness and anaesthesia signal pathways converge.

TRPA1 and TRPV1 contribute to propofol-mediated antagonism of U46619-induced constriction in murine coronary arteries

TRPA1 and TRPV1 appear to contribute to the propofol-mediated antagonism of U46619-induced constriction in murine coronary microvessels that involves activation of NOS and BKCa.

Orexin A Inhibits Propofol-Induced Neurite Retraction by a Phospholipase D/Protein Kinase Cε-Dependent Mechanism in Neurons

Rho-kinase is essential for propofol-induced neurite retraction in cortical neuronal cells and this inhibitory effect could be prevented by FIPI, staurosporine and PKCε translocation inhibitor peptide.

Angiotensin II-mediated suppression of synaptic proteins in mouse hippocampal neuronal HT22 cell was inhibited by propofol: role of calcium signaling pathway

Ang II, via AT1 receptor, induced oxidative stress and reduced the expression of synapsin I and PSD95 in HT22 cells, and propofol-mediated effects were alleviated by calcium chelator, CaMKII inhibitor, and PKCβ inhibitor.

Paradoxic effects of propofol on visceral pain induced by various TRPV1 agonists

Results suggest that propofol binds to TRPV1 at the capsaicin-binding pocket, and may increase visceral nociception induced by TRP V1 agonists via sensitization of TRpV1.

Propofol Causes Vasodilation In Vivo via TRPA1 Ion Channels: Role of Nitric Oxide and BKCa Channels

It is demonstrated for the first time that propofol-induced depressor responses in vivo are predominantly mediated by TRPA1 ion channels with no involvement of TRPV 1 ion channels and includes activation of both NOS and BKCa channels.

TRPA1 is functionally co-expressed with TRPV1 in cardiac muscle: Co-localization at z-discs, costameres and intercalated discs

Function expression and the precise ultrastructural localization of TRPA1 and TRPV1 ion channels are demonstrated in freshly isolated mouse CMs and both channels are expressed throughout the endocardium, myocardium and epicardium.

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