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Ionic Mechanism Underlying Rebound Depolarization in Medial Prefrontal Cortex Pyramidal Neurons
Przemysław Kurowski1, Katarzyna Grzelka1, Paweł Szulczyk1
1Laboratory of Physiology and Pathophysiology, Center for Preclinical Research and Technology, The Medical University of Warsaw, Warsaw, Poland.
Frontiers in Cellular Neuroscience
|May 10, 2018
Summary
Rebound depolarization (RD) in medial prefrontal cortex neurons is triggered by a sodium current, not potassium currents. This finding clarifies the ionic basis of RD, which converts inhibitory signals into excitation.
Area of Science:
- Neuroscience
- Cellular Electrophysiology
Background:
- Rebound depolarization (RD) transforms inhibitory signals into neuronal excitation.
- The precise ionic mechanisms underlying RD in specific neuronal types remain incompletely understood.
Purpose of the Study:
- To elucidate the ionic mechanisms of RD in synaptically isolated layer V medial prefrontal cortex (mPFC) pyramidal neurons.
- To investigate the roles of sodium and potassium currents in RD generation.
Main Methods:
- Electrophysiological recordings from rat mPFC pyramidal neurons.
- Pharmacological manipulation including BK channel blockers (paxilline), Ca++ removal/blockade, and protein kinase C (PKC) activation.
- Ionic substitution experiments (Na+ removal) and antibody application (anti-Nav1.9).
Main Results:
- RD was reliably evoked by hyperpolarization below -80 mV for >150 ms in 91% of neurons.
- RD required blockade of BK channels and was dependent on Na+ influx, being abolished by Na+ removal or anti-Nav1.9 antibody.
- RD was resistant to tetrodotoxin (TTX), indicating involvement of TTX-resistant sodium channels.
Conclusions:
- RD is primarily mediated by a low-threshold, TTX-resistant Na+ current.
- An opposing outward K+ current through BK channels normally limits RD.
- Conditions favoring RD, such as low extracellular Ca++ or PKC activation, may influence neuronal excitability and seizure susceptibility.
Keywords:
BK channelsCa++ channelsNav1.9 channelsamyloid β-peptide (1–42)prefrontal cortexpyramidal neuronsratsrebound depolarizationMore Related Videos
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