Skip to search boxSkip to navigationSkip to main content

Differential signaling of glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor in cultured ventral mesencephalic neurons

  • L. Feng
    ,
  • C. Y. Wang
    ,
  • H. Jiang
    ,
  • C. Oho
    ,
  • M. Dugich-Djordjevic
    ,
  • Lin Mei
*Corresponding author for this work
  • National Institutes of Health
    ,
  • Chinese Academy of Sciences
    ,
  • George Washington University
    ,
  • University of Virginia
    ,
Scholary Output:
Contribution to journal
Article
Peer-review

Abstract

In the ventral mesencephalon, two neurotrophic factors, brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor, have been shown previously to have similar effects on the survival of dopaminergic neurons. Here, we compared the signaling mechanisms for brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor, focusing on the mitogen-associated protein kinase and the transcription factor cyclic- AMP responsive element-binding protein. Double-staining experiments indicated that many neurons co-expressed the receptors for glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor, c-RET and TrkB, suggesting that they are responsive to both brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor. Although both brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor induced a rapid phosphorylation of mitogen-associated protein kinase and cyclic-AMP responsive element-binding protein, there were significant differences in the kinetics and pharmacology of the phosphorylation. The phosphorylation of mitogen-associated protein kinase by glial cell line-derived neurotrophic factor was transient; within 2 h, the level of mitogen-associated protein kinase phosphorylation returned to baseline. In contrast, the effect of brain-derived neurotrophic factor was long lasting; the mitogen-associated protein kinase remained phosphorylated for up to 4 h after brain-derived neurotrophic factor treatment. PD098059, a specific inhibitor for mitogen- associated protein kinase kinase, completely blocked the glial cell line- derived neurotrophic factor signaling through mitogen-associated protein kinase, but had no effect on brain-derived neurotrophic factor-induced mitogen-associated protein kinase phosphorylation. Both brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor induced the phosphorylation of cyclic-AMP responsive element-binding protein in the nuclei of ventral mesencephalon neurons. However, PD098059 blocked the cyclic-AMP responsive element-binding protein phosphorylation induced by glial cell line-derived neurotrophic factor, but not that by brain-derived neurotrophic factor. These results indicate that, although both brain- derived neurotrophic factor and glial cell line-derived neurotrophic factor act on ventral mesencephalon neurons, the two factors have different signaling mechanisms, which may mediate their distinctive biological functions.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 265-273 (9 pages)

Journal (Volume, Issue Number)

Neuroscience (Volume 93, Issue 1)

Publication milestones

  • Published - 06/1999

Publication status

Published - 06/1999

ISSN

0306-4522

Publication IDs

  • Scopus: 0033063448
  • PubMed: 10430490

Publication metrics

Metrics

SciVal
FWCI
0.69
SciVal
Author count
7
SciVal
citations
33
SciVal
Paper percentile
79
Scopus
citations
Fractional count
1
Fractional count
0.14
Fractional count
6
Fractional count
0.86
Fractional count
1
Fractional count
1

PlumX, opens in new tab

Citation count
31
Captures
22

Funding Details

We wish to thank Dr Yi Rao, and members of the Lu lab, for helpful discussions and critical comments on the manuscript. This work was supported in part by a grant from the Shanghai Science and Technology Commission and the National Natural Science Foundation of China.
FundersFunding number
NICHD
Z01HD000714
NSFC
-
STCSM
-