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Fluorescent Calcium Imaging and Subsequent In Situ Hybridization for Neuronal Precursor Characterization in Xenopus laevis

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Decrease in calcium concentration triggers neuronal retinoic acid synthesis during homeostatic synaptic plasticity.

Hui-Li Wang¹, Zhenjie Zhang, Maik Hintze

¹Stanford Institute of Neuro-Innovation and Translational Neuroscience and Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California 94305-5453, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience

|December 14, 2011

Summary

This summary is machine-generated.

Decreased postsynaptic calcium entry triggers all-trans retinoic acid (RA) synthesis, which is essential for homeostatic plasticity and increased AMPA receptor function in neurons.

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Area of Science:

Neuroscience
Cell Biology
Synaptic Plasticity

Background:

Homeostatic plasticity compensates for synaptic activity changes.
All-trans retinoic acid (RA) is known to increase AMPA receptor synthesis during plasticity.
The specific trigger for RA synthesis during homeostatic plasticity was previously unidentified.

Purpose of the Study:

To identify the synaptic signal that initiates all-trans retinoic acid (RA) synthesis.
To elucidate the role of postsynaptic calcium (Ca2+) in regulating RA synthesis and homeostatic plasticity.
To investigate the cell-autonomous function of RA in synaptic transmission.

Main Methods:

Activity-blockade protocols to induce homeostatic synaptic plasticity.
Manipulation of postsynaptic Ca2+ entry using chelators and L-type Ca2+-channel blockers.
Expression of modified L-type Ca2+ channels to assess cell autonomy.

Main Results:

RA synthesis is activated by significant decreases in postsynaptic Ca2+ entry.
Ca2+ influx acts as an inhibitor of RA synthesis.
RA is required for the upregulation of synaptic strength during homeostatic plasticity.
RA acts in a cell-autonomous manner to modulate synaptic transmission.

Conclusions:

Reduced resting Ca2+ levels in inactive neurons stimulate RA synthesis, driving homeostatic plasticity.
Modest basal Ca2+ levels in active neurons physiologically suppress RA synthesis.
This mechanism highlights a novel role for Ca2+ in regulating synaptic scaling via RA.