Propofol inhibited the delayed rectifier potassium current (Ik) via activation of protein kinase C epsilon in rat parietal cortical neurons

Song, Chun-yu; Xi, Hongjie; Liu, Yang; Qu, Lihui; Yue, Ziyong; Zhou, Jin; Cui, Xiaoqian; Wang, Nan; Pan, Zhenwei; Li, Wenzhi

doi:10.1016/j.ejphar.2010.10.072

Cited by 16 publications

(8 citation statements)

References 37 publications

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“…Application of the PKC agonist PMA increased the cloned human slowly activating delayed recti er K + current in HEK293 cells, but the PKCε peptide activator inhibited the current [28]. Some reports suggest that I K is inhibited by the activation of PKC in rat parietal cortical neurons and trigeminal ganglion neurons and juvenile guinea pig isolated hippocampal neurons [13,29,30]. The present study found that the activation of PKC inhibited I K in the hippocampal neurons.…”

Section: Discussionsupporting

confidence: 41%

Effect of transient receptor potential vanilloid 4 activation on the delayed rectifier potassium current in the hippocampal pyramidal neurons and Kv subunit expression in the hippocampi of mice

Zhou

et al. 2020

Preprint

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Activation of transient receptor potential vanilloid 4 (TRPV4) can increase hippocampal neuronal excitability. Recent studies have reported that TRPV4 may be involved in the pathogenesis of epilepsy. Voltage-gated potassium channels (VGPCs) play an important role in regulating neuronal excitability and abnormal VGPCs expression or function is related to epilepsy. Activation of TRPV4 can modulate ion channels, but whether activation of it could modulate VGPCs in hippocampal neurons remains unknown. Here we examined the effect of TRPV4 activation on the delayed rectifier potassium current (IK) in the hippocampal pyramidal neurons and on the Kv subunits expression. We also explored the role of TRPV4 in changes in Kv subunits expression in mice following pilocarpine-induced status epilepticus (PISE). Application of TRPV4 agonists, GSK1016790A and 5,6-EET, markedly reduced IK in the hippocampal pyramidal neurons, shifted the voltage-dependent inactivation curve to the hyperpolarization direction, and had no effect on the voltage-dependent activation curve. GSK1016790A- and 5,6-EET-induced inhibition of IK was blocked by TRPV4 specific antagonists, HC-067047 and RN1734. GSK1016790A-induced inhibition of IK was markedly attenuated by calcium/calmodulin-dependent kinase II (CaMKII) antagonist, but was not affected by protein kinase C or protein kinase A antagonists. Application of GSK1016790A for up to 1 h did not change the hippocampal protein levels of Kv1.1, Kv1.2, or Kv2.1. Intracerebroventricular injection of GSK1016790A for 3 d reduced the hippocampal protein levels of Kv1.2 and Kv2.1, leaving that of Kv1.1 unchanged. Kv1.2 and Kv2.1 protein levels were reduced markedly in hippocampi on day 3 post PISE, which was significantly reversed by HC-067047. We conclude that activation of TRPV4 inhibits IK in the hippocampal pyramidal neurons, possibly by activating CaMKII. Persistent activation of TRPV4 decreased Kv1.2 and Kv2.1 expression, which may be associated with the decrease in Kv1.2 and Kv2.1 expression following PISE.

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Section: Discussionsupporting

confidence: 41%

Effect of transient receptor potential vanilloid 4 activation on the delayed rectifier potassium current in the hippocampal pyramidal neurons and Kv subunit expression in the hippocampi of mice

Zhou

et al. 2020

Preprint

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“…Recent results show propofol can inhibit I K via the activation of PKC epsilon in rat cerebral parietal cortical neurons [42].…”

Section: Pkc ε Modulates Ion Channelsmentioning

confidence: 99%

The role of protein kinase C epsilon in neural signal transduction and neurogenic diseases

Chen

Tian

2011

Front. Med.

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Protein kinase C epsilon (PKC ɛ) is one of major isoforms in novel PKC family. Although it has been extensively characterized in the past decade, the role of PKC ɛ in neuron is still not well understood. Advances in molecular biology have now removed significant barriers to the direct investigation of PKC ɛ functions in vivo, and PKC ɛ has been increasingly implicated in the neural biological functions and associated neurogenic diseases. Recent studies have provided important insights into the influence of PKC ɛ on cortical processing at both the single cell level and network level. These studies provide compelling evidence that PKC ɛ could regulate distinct aspects of neural signal transduction and suggest that the coordinated actions of a number of molecular signals contribute to the specification and differentiation of PKC ɛ signal pathway in the developing brain.

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“…Whole K + current in cultured neurons of murine colliculi and I K in the trigeminal ganglion neurons have been reported to be inhibited by cAMP‐dependent PKA activation (Chen et al., 2008; Fagni et al., 1992). Activation of PKC has been proven to inhibit I K in rat parietal cortical neurons and trigeminal ganglion neurons and juvenile guinea pig isolated hippocampal neurons (Chen et al., 2008; Doerner et al., 1988; Song et al., 2018). Similarly, in the present study, I K recorded in the hippocampal pyramidal neurons was inhibited by the activation of PKA and PKC.…”

Section: Discussionmentioning

confidence: 99%

Transient receptor potential vanilloid 4 activation inhibits the delayed rectifier potassium channels in hippocampal pyramidal neurons: An implication in pathological changes following pilocarpine‐induced status epilepticus

Zhou

et al. 2020

J of Neuroscience Research

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Activation of transient receptor potential vanilloid 4 (TRPV4) can increase hippocampal neuronal excitability. TRPV4 has been reported to be involved in the pathogenesis of epilepsy. Voltage-gated potassium channels (VGPCs) play an important role in regulating neuronal excitability and abnormal VGPCs expression or function is related to epilepsy. Here, we examined the effect of TRPV4 activation on the delayed rectifier potassium current (I K) in hippocampal pyramidal neurons and on the Kv subunits expression in male mice. We also explored the role of TRPV4 in changes in Kv subunits expression in male mice following pilocarpine-induced status epilepticus (PISE). Application of TRPV4 agonists, GSK1016790A and 5,6-EET, markedly reduced I K in hippocampal pyramidal neurons and shifted the voltage-dependent inactivation curve to the hyperpolarizing direction. GSK1016790A-and 5,6-EET-induced inhibition of I K was blocked by TRPV4 specific antagonists, HC-067047 and RN1734. GSK1016790Ainduced inhibition of I K was markedly attenuated by calcium/calmodulin-dependent kinase II (CaMKII) antagonist. Application of GSK1016790A for up to 1 hr did not change the hippocampal protein levels of Kv1.1, Kv1.2, or Kv2.1. Intracerebroventricular injection of GSK1016790A for 3 d reduced the hippocampal protein levels of Kv1.2 and Kv2.1, leaving that of Kv1.1 unchanged. Kv1.2 and Kv2.1 protein levels as well as I K reduced markedly in hippocampi on day 3 post PISE, which was significantly reversed by HC-067047. We conclude that activation of TRPV4 inhibits I K in hippocampal pyramidal neurons, possibly by activating CaMKII. TRPV4-induced decrease in Kv1.2 and Kv2.1 expression and I K may be involved in the pathological changes following PISE.

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Propofol inhibited the delayed rectifier potassium current (Ik) via activation of protein kinase C epsilon in rat parietal cortical neurons

Cited by 16 publications

References 37 publications

Effect of transient receptor potential vanilloid 4 activation on the delayed rectifier potassium current in the hippocampal pyramidal neurons and Kv subunit expression in the hippocampi of mice

Effect of transient receptor potential vanilloid 4 activation on the delayed rectifier potassium current in the hippocampal pyramidal neurons and Kv subunit expression in the hippocampi of mice

The role of protein kinase C epsilon in neural signal transduction and neurogenic diseases

Transient receptor potential vanilloid 4 activation inhibits the delayed rectifier potassium channels in hippocampal pyramidal neurons: An implication in pathological changes following pilocarpine‐induced status epilepticus

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