May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Glutamate Regulates Progenitor Cells Proliferation During Retinal Development
Author Affiliations & Notes
  • R.A. Martins
    Developmental Neurobiology, St Jude Children Research Hospital, Memphis, TN
    Neurogenesis Lab, IBCCF, UFRJ, Rio de Janeiro, Brazil
  • R. Linden
    Neurogenesis Lab, IBCCF, UFRJ, Rio de Janeiro, Brazil
  • M. Dyer
    Developmental Neurobiology, St Jude Children Research Hospital, Memphis, TN
  • Footnotes
    Commercial Relationships  R.A. Martins, None; R. Linden, None; M. Dyer, None.
  • Footnotes
    Support  NIH, NSF, NCI, Pew Scholars, RPB
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 4004. doi:
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      R.A. Martins, R. Linden, M. Dyer; Glutamate Regulates Progenitor Cells Proliferation During Retinal Development . Invest. Ophthalmol. Vis. Sci. 2005;46(13):4004.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract
 
Abstract:
 

Glutamate, the main excitatory neurotransmitter of the adult CNS, is also important for the control of cell proliferation, survival and differentiation during CNS development. Glutamate exerts an antiproliferative effect upon neuronal and glial progenitors from developing cortex and cerebellum. However, the molecular mechanism mediating these effects is not fully understood.

 

In this work, we asked whether glutamate regulates cell proliferation during retinal development and the molecular mechanisms of cell cycle involved in this effect.

 

Progenitor cells from embryonic retina express glutamate receptors as observed by RT–PCR and immunocitochemistry. Treatment of retinal explants with glutamate resulted in a dose–dependent decrease in the number of BrdU–labeled cells, while the AMPA/Kainate receptor antagonist, NBQX, had the opposite effect. Consistently, clonal analysis using replication–incompetent retrovirus, revealed that glutamate favors the formation of smaller clones (figure) and blockade of AMPA/Kainate receptors increase the proportion of larger clones. Glutamate receptor activation did not change the expression levels of cell cycle–regulating molecules, as observed by RT–PCR and western blot. But, interestingly, preliminary data demonstrate that glutamate inhibits the CDK2–associated kinase activity.

 

Our data show that glutamate regulates retinal progenitor proliferation through AMPA/Kainate receptors and suggest a cell cycle mechanism responsible for this effect. This work provides evidence about how extrinsic factors, such as glutamate, drive cell cycle intrinsic machinery regulating neuronal proliferation during development. $graphic_{5D2F4E85–3E38–4D52–9801–1210013B25E4}$$

 

 

 
Keywords: excitatory amino acid receptors • neurotransmitters/neurotransmitter systems • proliferation 
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