Activation of protein kinase C and inositol 1,4,5-triphosphate receptors antagonistically modulate voltage-gated sodium channels in striatal neurons

Hourez, Raphaël; Azdad, Karima; Vanwalleghem, Gilles; Roussel, Céline; Gall, David; Schiffmann, Serge N.

doi:10.1016/j.brainres.2005.08.031

Cited by 14 publications

(8 citation statements)

References 45 publications

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“…These findings are consistent with the generally-accepted opinion that water and sodium tend to coexist, and move together through the plasma membrane under physiological and pathological conditions (Gotoh et al, 1985;Loo et al, 1996;Wright and Loo, 2000). Alternatively, in addition to the blunting of AQP4 upregulation by PMA, brain sodium channels may have been independently affected (Hourez et al, 2005).…”

Section: Discussionsupporting

confidence: 89%

The Protein Kinase C Activator Phorbol Myristate Acetate Decreases Brain Edema by Aquaporin 4 Downregulation after Middle Cerebral Artery Occlusion in the Rat

Fazzina

Amorini

Marmarou

et al. 2010

Journal of Neurotrauma

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The protein kinase C activator phorbol 12-myristate 13-acetate (PMA) is known to interact with aquaporin 4 (AQP 4), a water-selective transporting protein that is abundant in astrocytes, and has experimentally been found to decrease osmotically-induced cell swelling. The purpose of this study was to examine whether PMA reduces brain edema following focal ischemia induced by middle cerebral artery (MCA) occlusion by modulation of AQP4 expression. Male Sprague-Dawley rats were randomly assigned to either sham surgery (n ¼ 6), or a continuous intravenous infusion of vehicle (1% dimethylsulfoxide), followed by MCA occlusion (n ¼ 18), and administration of PMA at 50 mg=kg (n ¼ 6) or at 200 mg=kg (n ¼ 6) starting 60 min before or 30 min (200 mg=kg; n ¼ 6) or 60 min (200 mg=kg; n ¼ 6) after MCA occlusion. Cerebral blood flow was monitored with laser Doppler over the MCA territory, and confirmed a 70% reduction during occlusion. After a 2-h period of ischemia and 2 h of reperfusion, the animals were sacrificed for assessment of brain water content and sodium and potassium concentration. AQP4 expression was assessed by immunoblotting and quantified by densitometry (n ¼ 24). Statistical analysis was performed by ANOVA followed by Tukey's post-hoc test. PMA treatment at 200 mg=kg significantly reduced brain water concentration in the infarcted area when started 60 min before or 30 min after occlusion ( p < 0.001 and p ¼ 0.022, respectively), and prevented the subsequent sodium shift ( p < 0.05). PMA normalized the AQP4 upregulation in ischemia ( p ¼ 0.021). A downregulation of AQP4 in the ischemic area paralleling the reduction in brain edema formation following PMA treatment suggests that the effect was mediated by AQP4 modulation.

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Section: Discussionsupporting

confidence: 89%

The Protein Kinase C Activator Phorbol Myristate Acetate Decreases Brain Edema by Aquaporin 4 Downregulation after Middle Cerebral Artery Occlusion in the Rat

Fazzina

Amorini

Marmarou

et al. 2010

Journal of Neurotrauma

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“…All these mechanisms share the common theme that different phosphorylation sites control different aspects of channel gating. Even voltage-gated sodium channels, long thought not to be modulated, are now known to respond to a wide variety of modulators [78] which target multiple phosphorylation sites at the α-subunits [79–81]. The sensitivity to multiple signaling pathways suggests a balanced modulation by many neuromodulators.…”

Section: Neuromodulation Of Neuronal Excitabilitymentioning

confidence: 99%

Neuromodulation of neurons and synapses

Nadim

Bucher

2014

Current Opinion in Neurobiology

257

230

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Neuromodulation underlies the flexibility of neural circuit operation and behavior. Individual neuromodulators can have divergent actions in a neuron by targeting multiple physiological mechanisms. Conversely, multiple neuromodulators may have convergent actions through overlapping targets. Additionally, the divergent and convergent neuromodulator actions can be unambiguously synergistic or antagonistic. Neuromodulation often entails balanced adjustment of nonlinear membrane and synaptic properties by targeting ion channel and synaptic dynamics rather than just excitability or synaptic strength. In addition, neuromodulators can exert effects at multiple timescales, from short-term adjustments of neuron and synapse function to persistent long-term regulation. This short review summarizes some highlights of the diverse actions of neuromodulators on ion channel and synaptic properties.

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“…The two pathways are activated by many biological compounds, such as prostaglandin E 2 , bradykinin and serotonin, and then enhance the function of TTX-R channels inducing inflammatory hyperalgesia (Cardenas et al, 1997; Gold et al, 1998; Ikeda et al, 2005; Smith et al, 2000). Other pathways such as PKG (Renganathan et al, 2002) and lipid cascade (Hourez et al, 2005) have also been reported to participate in modulating the function of VGSCs. Our previous study shows that anisotonicity can sensitize capsaicin evoked current ( I caps ) via different intracellular pathways (Liu et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Changes in osmolality modulate voltage-gated sodium channels in trigeminal ganglion neurons

Chen

Liu

et al. 2009

Neuroscience Research

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Voltage-gated sodium channels (VGSCs) are important channels which participate in many physiological functions. Whether VGSCs can be modulated by changes in osmolality in trigeminal ganglion (TG) neurons remains unknown. In this study, by using whole-cell patch clamp techniques, we tested the effects of hypo-and hypertonicity on VGSCs in cultured TG neurons. Our data show that tetrodotoxin-resistant sodium current (TTX-R current) was inhibited in the presence of hypoand hypertonic solutions. In hypertonic solutions both voltage-dependent activation and inactivation curves shifted to the hyperpolarizing direction, while in hypotonic solutions only inactivation curve shifted to the hyperpolarizing direction. Transient Receptor Potential Vanilloid 4 receptor (TRPV4) activator mimicked the inhibition of TTX-R current by hypotonicity and the inhibition by hypotonicity was markedly attenuated by TRPV4 receptor blocker and in TRPV4 -/-mice TG neurons. We also demonstrate that inhibition of PKA selectively attenuated hypotonicity-induced inhibition, whereas antagonism of PLC and PI3K selectively attenuated hypertonicity-induced inhibition. We conclude that although hypo-and hypertonicity have similar effect on VGSCs, receptor and intracellular signaling pathways are different for hypo-versus hypertonicity-induced inhibition of TTX-R current.

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Activation of protein kinase C and inositol 1,4,5-triphosphate receptors antagonistically modulate voltage-gated sodium channels in striatal neurons

Cited by 14 publications

References 45 publications

The Protein Kinase C Activator Phorbol Myristate Acetate Decreases Brain Edema by Aquaporin 4 Downregulation after Middle Cerebral Artery Occlusion in the Rat

The Protein Kinase C Activator Phorbol Myristate Acetate Decreases Brain Edema by Aquaporin 4 Downregulation after Middle Cerebral Artery Occlusion in the Rat

Neuromodulation of neurons and synapses

Changes in osmolality modulate voltage-gated sodium channels in trigeminal ganglion neurons

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