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Glutamate regulates retinal progenitors cells proliferation during development
Rodrigo A P Martins1, Rafael Linden, Michael A Dyer
1Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
The European Journal of Neuroscience
|August 24, 2006
Summary
Glutamate, an excitatory neurotransmitter, controls retinal progenitor cell proliferation during embryonic development. It reduces cell division by post-translationally modulating cyclin/Cdk2 kinase activity, impacting retinal cell fate.
Area of Science:
- Neuroscience
- Developmental Biology
- Cell Biology
Background:
- Precise cell cycle exit and fate specification are crucial for retinal development.
- Neurotransmitters are increasingly recognized for their role in early central nervous system development.
- Glutamate's role in regulating retinal progenitor cell proliferation was investigated.
Purpose of the Study:
- To determine if glutamate influences retinal progenitor cell proliferation during embryonic development.
- To elucidate the mechanism by which glutamate affects cell cycle progression.
Main Methods:
- Exposure of embryonic mouse retinal progenitor cells to exogenous glutamate.
- Analysis of cell proliferation, cell death, and the p53 pathway.
- Utilized replication-incompetent retrovirus for clonal analysis.
- Performed real-time reverse transcriptase-polymerase chain reaction and immunoblot analyses.
- Assessed Cdk2 kinase activity.
Main Results:
- Exogenous glutamate decreased retinal progenitor cell proliferation in a dose-dependent manner without inducing cell death or activating p53.
- Activation of AMPA/kainate receptors led to premature cell cycle exit.
- Blockade of AMPA/kainate receptors resulted in larger clonal expansions, indicating long-term proliferation effects.
- Glutamate did not alter G1/S-phase regulatory mRNA or protein levels.
- Glutamate reduced Cdk2 kinase activity.
Conclusions:
- Glutamate regulates retinal progenitor cell proliferation during embryonic development.
- The mechanism involves the post-translational modulation of cyclin/Cdk2 kinase activity.
- Modulating glutamatergic activity has significant consequences on retinal cell proliferation and development.
