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Fluorescent Calcium Imaging and Subsequent In Situ Hybridization for Neuronal Precursor Characterization in Xenopus laevis
Published on: February 18, 2020
Calcium-dependent phosphorylation regulates neuronal stability and plasticity in a highly precise pacemaker nucleus
Andrew A George1, Gregory T Macleod, Harold H Zakon
1Section of Neurobiology and Institute for Neuroscience, Patterson Laboratory, University of Texas at Austin, Texas, USA. ageorge@biology2.wustl.edu
Journal of Neurophysiology
|April 29, 2011
Summary
This study reveals how neuronal plasticity interacts with stability mechanisms. Protein Kinase C (PKC) regulates stable firing, while calcineurin controls plasticity duration, offering a general model for neuronal excitability.
Area of Science:
- Neuroscience
- Cellular Biology
- Electrophysiology
Background:
- Neuronal excitability exhibits both stable properties and adaptive plasticity.
- Interactions between pathways maintaining stability and those driving plasticity are poorly understood.
- Pacemaker neurons in electric fish display stable firing and N-methyl-D-aspartate (NMDA) receptor-dependent plasticity.
Purpose of the Study:
- Investigate the interplay between cellular pathways governing neuronal stability and plasticity.
- Elucidate the mechanisms underlying NMDA receptor-dependent plasticity in pacemaker neurons.
- Propose a general model for activity-dependent regulation of neuronal excitability.
Main Methods:
- Electrophysiological recordings of pacemaker neurons in weakly electric fish.
- Pharmacological manipulation of protein kinase C (PKC) and calcineurin pathways.
- Analysis of N-methyl-D-aspartate (NMDA) receptor function and calcium signaling.
Main Results:
- Basal firing rates are modulated by a serial interaction of conventional and atypical PKC isoforms, establishing individual differences.
- NMDA receptor-dependent plasticity involves further activation of PKC pathways, which are primed in an unsaturated state.
- Calcineurin regulates the duration of plasticity, returning pacemaker firing rates to baseline.
Conclusions:
- Neuronal plasticity can be achieved by modulating existing stability mechanisms like PKC.
- Recruitment of alternative pathways, such as calcineurin, terminates plasticity and constrains excitability.
- This study proposes a general model for regulating activity-dependent changes in neuronal excitability.
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