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Updated: Jun 28, 2026
04:48
A High-throughput Calcium-flux Assay to Study NMDA-receptors with Sensitivity to Glycine/D-serine and Glutamate
Published on: July 10, 2018
Dendritic NMDA receptors activate axonal calcium channels
Jason M Christie1, Craig E Jahr
1Vollum Institute, Oregon Health & Science University, Portland, OR 97239-3098, USA. christij@ohsu.edu
Neuron
|October 30, 2008
Summary
Activation of NMDA receptors (NMDARs) in cerebellar stellate cells influences transmitter release indirectly. Dendritic NMDAR activation causes depolarization, opening voltage-sensitive Ca(2+) channels in axons to modulate presynaptic Ca(2+) levels.
Area of Science:
- Neuroscience
- Cellular Biology
- Synaptic Plasticity
Background:
- NMDA receptors (NMDARs) regulate synaptic strength by affecting neurotransmitter release.
- NMDARs' permeability to Ca(2+) suggests roles in presynaptic Ca(2+) increase or axonal depolarization.
- Understanding NMDAR function is crucial for deciphering neuronal communication.
Purpose of the Study:
- To investigate the mechanism by which NMDAR activation influences presynaptic Ca(2+) and transmitter release in cerebellar stellate cells.
- To determine the localization and functional expression of NMDARs in these neurons.
Main Methods:
- Two-photon microscopy was employed to measure Ca(2+) dynamics in axon varicosities.
- Somatic depolarization and focal activation of dendritic NMDARs were used to probe NMDAR function.
- Electrophysiological recordings assessed the spread of depolarization.
Main Results:
- Somatic depolarization and dendritic NMDAR activation induced Ca(2+) transients in axon varicosities.
- These axonal Ca(2+) transients were mediated by voltage-sensitive Ca(2+) channels (VSCCs) activated by electrotonic spread of depolarization.
- Direct activation of NMDARs on axons was not detected, suggesting somatodendritic expression.
Conclusions:
- Functional NMDARs are exclusively expressed in the somatodendritic compartment of cerebellar stellate cells.
- Dendritic NMDAR activation indirectly influences presynaptic Ca(2+) and release via axonal VSCCs.
- This indirect mechanism may play a role in presynaptic plasticity and neurotransmitter release modulation.
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