Neuromodulation of Na+ channels: An unexpected form of cellular platicity

@article{Cantrell2001NeuromodulationON,
  title={Neuromodulation of Na+ channels: An unexpected form of cellular platicity},
  author={Angela R. Cantrell and William A. Catterall},
  journal={Nature Reviews Neuroscience},
  year={2001},
  volume={2},
  pages={397-407}
}
Voltage-gated Na+ channels set the threshold for action potential generation and are therefore good candidates to mediate forms of plasticity that affect the entire neuronal output. Although early studies led to the idea that Na+ channels were not subject to modulation, we now know that Na+ channel function is affected by phosphorylation. Furthermore, Na+ channel modulation is implicated in the control of input–output relationships in several types of neuron and seems to be involved in… Expand
Neuromodulation of Sodium Channels
Voltage-gated Na+ channels are phosphorylated on a family of interacting sites by cAMP-dependent protein kinase and protein kinase C, which is stimulated by activation of receptors forExpand
Endogenous polyamines regulate cortical neuronal excitability by blocking voltage-gated Na+ channels
TLDR
It is found that products of PA metabolism, the ubiquitous aliphatic polycations spermine and spermidine, are endogenous blockers of Na+ channels in layer 5 pyramidal cells, and that changes in PA levels profoundly modify Na+ channel availability and thereby shape the integrative behavior of single neurons and neocortical circuits. Expand
Transmitter Modulation of Slow, Activity-Dependent Alterations in Sodium Channel Availability Endows Neurons with a Novel Form of Cellular Plasticity
TLDR
The results described here show that both GPCR- and protein kinase-dependent reductions in Na+ channel availability are mediated by a slow, voltage-dependent process with striking similarity to slow inactivation, an intrinsic gating mechanism of Na+ channels. Expand
Distinctive Properties and Powerful Neuromodulation of Nav1.6 Sodium Channels Regulates Neuronal Excitability
TLDR
The role of Nav1.6 in neuronal function is examined and a thorough review of this channel’s complex regulatory mechanisms and how they may contribute to neuromodulation is provided. Expand
Na+ channel blockers for the treatment of pain: Context is everything, almost
  • M. Gold
  • Medicine
  • Experimental Neurology
  • 2008
TLDR
Functional diversity and selective expression patterns of channel types indicate that it may be possible to selectively block persistent pain associated with peripheral tissue injury. Expand
Voltage-gated sodium channels and hyperalgesia.
TLDR
The discrete localization of the tetrodotoxin (TTX)-resistant channels, in particular NaV1.8, in the peripheral nerves may provide a novel opportunity for the development of a drug targeted at these channels to achieve efficacious pain relief with an acceptable safety profile. Expand
Activity-dependent modulation of neuronal sodium channel expression / by Joshua Peter Klein.
Action potentials initiate via the voltage-dependent opening of plasma membrane-associated sodium channels. The number and type of sodium channels in a neuronal membrane determine the quantity ofExpand
Functional properties and differential neuromodulation of Nav1.6 channels
TLDR
The unique properties of Na(V)1.6 channels, together with the resurgent currents that they conduct in neurons, make these channels well-suited to provide the driving force for sustained repetitive firing, a crucial property of neurons. Expand
Kv2.1: a voltage-gated k+ channel critical to dynamic control of neuronal excitability.
TLDR
Previous studies of Kv2.1 localization and function in neurons are reviewed, recent work regarding dynamic regulation of these characteristics are summarized, and possible roles of the Kv 2.1 channel in neuronal and network excitability are discussed. Expand
Voltage-gated sodium channels and their roles in drug action
TLDR
The physiological roles of voltage-gated sodium channels, their molecular classification, structure and modulation by drugs are explained and potential targets for contribution to the clinical state of anaesthesia are identified. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 133 REFERENCES
Voltage-Dependent Neuromodulation of Na+ Channels by D1-Like Dopamine Receptors in Rat Hippocampal Neurons
TLDR
It is reported that neuromodulation of Na+ currents by DA receptors via PKA is voltage-dependent in the range of −110 to −70 mV and is also sensitive to concurrent activation of protein kinase C (PKC). Expand
Tetrodotoxin-resistant Na+ currents and inflammatory hyperalgesia.
  • M. Gold
  • Chemistry, Medicine
  • Proceedings of the National Academy of Sciences of the United States of America
  • 1999
TLDR
Data presented at the Neurobiology of Pain colloquium raised a number of interesting questions regarding the role of TTX-resistant Na+ currents in inflammatory hyperalgesia; implications of three of these questions are discussed. Expand
S-8-1: State-dependent regulation of neuronal excitability by dopamine
TLDR
The results and those of others suggest that D2-class receptors serve to make the transition to the depolarized 'upstate' from the hyperpolarization 'downstate' more probable in response to cortical input, which provides a mechanism by which dopamine could shape global striatal activity governing the execution of motor behaviors. Expand
Muscarinic Modulation of Sodium Current by Activation of Protein Kinase C in Rat Hippocampal Neurons
TLDR
Activation of endogenous muscarinic receptors on hippocampal neurons strongly modulates Na+ channel activity by activation of PKC, and cholinergic input from basal forebrain neurons may have this effect in the hippocampus in vivo. Expand
The molecular basis of neuronal excitability.
TLDR
The distribution of sodium channels among the functional compartments of the neuron is described and work leading to the identification, purification, and characterization of this membrane glycoprotein is reviewed. Expand
Structure and function of voltage‐gated sodium channels
TLDR
This paper reviews the links between sodium channel structure and function and finds that sodium channels bind local anaesthetics and various toxins and are subject to regulation at the levels of transcription, subunit interaction and post‐translational modification. Expand
Human neocortical excitability is decreased during anoxia via sodium channel modulation.
When the central nervous system in humans is deprived of oxygen, the effects are potentially disastrous. Electroencephalographic activity is lost and higher brain function ceases rapidly. Despite theExpand
Dopamine modulates a Ca2+-activated potassium conductance in mammalian hippocampal pyramidal cells
TLDR
It is reported here that DA causes prolonged inhibition associated with hyperpolarization and increased conductance, which would make DA effective in modulating the high frequency firing and burst generation which occurs normally in some neurones and pathologically in HPCs during epileptogenesis. Expand
Nomenclature of Voltage-Gated Sodium Channels
TLDR
The present alphabetical nomenclature does not reveal the structural relationships among the α1 subunits of Ca2+ channels, but it is apparent that these two alphabeticals will overlap at α1L, which may not mediate an L-type Ca2- current and therefore may create confusion. Expand
From Ionic Currents to Molecular Mechanisms The Structure and Function of Voltage-Gated Sodium Channels
TLDR
Together, these studies showed that the mechanisms of sodium channel function and regulation, purified sodium channel protein contained the essential and gives a perspective for future research on the ex-elements for ion conduction and voltage-dependent panding family of Sodium channel proteins. Expand
...
1
2
3
4
5
...