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Published on: October 1, 2007
FGF2 delays tectal neurogenesis, increases tectal cell numbers, and alters tectal lamination in embryonic chicks
Luke D McGowan1, Roula A Alaama, Georg F Striedter
1Department of Neurobiology and Behavior, Center for the Neurobiology of Learning and Memory, University of California Irvine, Irvine, California, United States of America.
Insights
Fibroblast growth factor 2 (FGF2) delays neurogenesis in embryonic chick brains, increasing optic tectum size. This delay impacts cell numbers and layer thickness, altering brain morphology.
Area of Science:
- Developmental neurobiology
- Molecular biology
- Cell biology
Background:
- Fibroblast growth factor 2 (FGF2) is known to enlarge the optic tectum in embryonic chicks.
- The precise mechanism behind this size increase has not been fully elucidated.
Purpose of the Study:
- To investigate the effect of FGF2 on neurogenesis in the embryonic chick optic tectum.
- To determine if FGF2-induced tectal enlargement is mediated by alterations in the timing of neurogenesis.
Main Methods:
- Intraventricular injection of FGF2 on embryonic day 4 (ED4).
- Cumulative labeling with thymidine analog EdU on ED5 and ED8 to track cell proliferation.
- Analysis of labeled and unlabeled cell populations in rostroventral and caudodorsal tectum.
Main Results:
- FGF2 treatment significantly reduced the proportion and number of unlabeled cells, indicating a delay in neurogenesis.
- This delay in neurogenesis persisted for several days after FGF2 administration.
- FGF2 treatment led to a more than doubling of tectal cell numbers and caused thinning of early-born tectal layers.
Conclusions:
- FGF2 delays neurogenesis throughout much of the embryonic chick optic tectum.
- This FGF2-induced delay in neurogenesis is the primary cause of increased tectum size and altered morphology.
- The findings provide insights into the regulation of brain development by growth factors.
Abstract:
Intraventricular injections of the fibroblast growth factor 2 (FGF2) are known to increase the size of the optic tectum in embryonic chicks. Here we show that this increase in tectum size is due to a delay in tectal neurogenesis, which by definition extends the proliferation of tectal progenitors. Specifically, we use cumulative labeling with the thymidine analog EdU to demonstrate that FGF2 treatment on embryonic day 4 (ED4) reduces the proportion and absolute number of unlabeled cells in the rostroventral tectum when EdU infusions are begun on ED5, as one would expect if FGF2 retards tectal neurogenesis. We also examined FGF2's effect on neurogenesis in the caudodorsal tectum, which is born 2-3 days after the rostroventral tectum, by combining FGF2 treatment on ED4 with EDU infusions beginning on ED8. Again, FGF2 treatment reduced the proportion and number of EdU-negative (i.e., unlabeled) cells, consistent with a delay in neurogenesis. Collectively, these data indicate FGF2 in embryonic chicks delays neurogenesis throughout much of the tectum and continues to do so for several days after the FGF2 injection. One effect of this delay in neurogenesis is that tectal cell numbers more than double. In addition, tectal laminae that are born early in development become abnormally thin and cell-sparse after FGF2 treatment, whereas late-born layers remain unaffected. Combined with the results of prior work, these data indicate that FGF2 delays tectal neurogenesis and, thereby, triggers a cascade of changes in tectum size and morphology.
