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Persistent sodium current in mammalian central neurons
1Department of Physiology and Biophysics, University of Washington, Seattle 98195, USA.
Annual Review of Physiology
|January 1, 1996
Summary
Mammalian neurons possess a persistent sodium current (INaP) crucial for synaptic activity, particularly in dendrites. Understanding INaP
Area of Science:
- Neuroscience
- Computational Neuroscience
- Cellular Electrophysiology
Background:
- Mammalian central nervous system (CNS) neurons exhibit a tetrodotoxin-sensitive sodium current with a noninactivating component (INaP).
- Despite its small amplitude (<1% of transient sodium current), INaP is functionally significant due to its activation at more negative potentials and high neuron input resistance.
Purpose of the Study:
- To investigate the functional significance and potential mechanisms of the noninactivating sodium current (INaP) in mammalian CNS neurons.
- To explore how INaP influences synaptic current transduction and neuronal excitability.
Main Methods:
- Electrophysiological recordings in mammalian CNS neurons.
- Analysis of voltage-gated sodium channel kinetics and function.
- Modeling of synaptic current integration with INaP.
Main Results:
- INaP is activated at potentials negative to the transient sodium current, where neuron input resistance is high.
- INaP contributes to synaptic current, especially in dendrites, enhancing the effectiveness of distal synaptic inputs.
- The precise mechanism of INaP (modal gating vs. distinct channel subtype) remains undetermined.
Conclusions:
- INaP plays a critical role in modulating neuronal excitability and synaptic integration in the mammalian CNS.
- Further research into the INaP mechanism is warranted to understand its full impact on neuronal function.
- Modulation of INaP represents a potential target for influencing neuronal signal processing.