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The Journal of Neuroscience, November 5, 2003, 23(31):10137-10145

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Development/Plasticity/Repair
TrkB Receptor Signaling Regulates Developmental Death Dynamics, But Not Final Number, of Retinal Ganglion Cells

Graeme S. Pollock,¹ Regine Robichon,¹ Kristina A. Boyd,¹ Kristi A. Kerkel,¹ Melissa Kramer,¹ Johnalyn Lyles,¹ Ranjini Ambalavanar,¹ Asema Khan,¹ David R. Kaplan,³ Robert W. Williams,⁴ and Douglas O. Frost^1,2

¹Department of Pharmacology and Experimental Therapeutics, ²Neuroscience Program, University of Maryland School of Medicine, Baltimore, Maryland 21201, ³Hospital for Sick Children, Department Cancer, Toronto, Ontario M5G 1X8, Canada, ⁴University of Tennessee Health Science Center, Department of Anatomy and Neurobiology, Memphis, Tennessee 38163

We investigated the effects of endogenous neurotrophin signaling on the death-survival of immature retinal ganglion cells (RGCs) in vivo. Null mutation of brain-derived neurotrophic factor [(BDNF) alone or in combination with neurotrophin 4 (NT4)] increases the peak rate of developmental RGC death as compared with normal. Null mutation of NT4 alone is ineffective. Null mutation of the full-length trkB (trkB_FL) receptor catalytic domain produces a dose-dependent increase in the peak RGC death rate that is negatively correlated with retinal levels of trkB_FL protein and phosphorylated (activated) trkB_FL. Depletion of target-derived trkB ligands by injection of trkB-Fc fusion protein into the superior colliculus increases the peak rate of RGC death compared with trkA-Fc-treated and normal animals. Adult trkB_FL^+/- mice have a normal number of RGCs, despite an elevated peak death rate of immature RGCs. Thus, target-derived BDNF modulates the dynamics of developmental RGC death through trkB_FL activation, but BDNF/trkB-independent mechanisms determine the final number of RGCs.

Key words: neurotrophin; visual system; apoptosis; mouse; hamster; retina; ganglion cell; development; cell death; trkB

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Received May 22, 2003; revised July 24, 2003; accepted July 27, 2003.

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