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The Journal of Neuroscience, January 21, 2009, 29(3):678-685; doi:10.1523/JNEUROSCI.5060-08.2009

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Development/Plasticity/Repair
Endogenous Truncated TrkB.T1 Receptor Regulates Neuronal Complexity and TrkB Kinase Receptor Function In Vivo

Laura Carim-Todd,^1 * Kevin G. Bath,^2 * Gianluca Fulgenzi,^1,3 Sudhirkumar Yanpallewar,¹ Deqiang Jing,² Colleen A. Barrick,¹ Jodi Becker,¹ Hannah Buckley,¹ Susan G. Dorsey,^1,4 Francis S. Lee,² and Lino Tessarollo¹

¹Neural Development Group, Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute, Frederick, Maryland 21702, ²Department of Psychiatry, Weill Cornell Medical College of Cornell University, New York, New York 10065, ³Department of Molecular Pathology, University of Marche, 60020 Ancona, Italy, and ⁴Organizational Systems and Adult Health, University of Maryland School of Nursing, Baltimore, Maryland 21201

Correspondence should be addressed to Dr. Lino Tessarollo, Neural Development Group, Mouse Cancer Genetics Program, National Cancer Institute–Frederick, 7th Street, Building 560, Room 32-31D, P.O. Box B, Frederick, MD 21702. Email: tessarol{at}mail.nih.gov

Pathological or in vitro overexpression of the truncated TrkB (TrkB.T1) receptor inhibits signaling through the full-length TrkB (TrkB.FL) tyrosine kinase receptor. However, to date, the role of endogenous TrkB.T1 is still unknown. By studying mice lacking the truncated TrkB.T1 isoform but retaining normal spatiotemporal expression of TrkB.FL, we have analyzed TrkB.T1-specific physiological functions and its effect on endogenous TrkB kinase signaling in vivo. We found that TrkB.T1-deficient mice develop normally but show increased anxiety in association with morphological abnormalities in the length and complexity of neurites of neurons in the basolateral amygdala. However, no behavioral abnormalities were detected in hippocampal-dependent memory tasks, which correlated with lack of any obvious hippocampal morphological deficits or alterations in basal synaptic transmission and long-term potentiation. In vivo reduction of TrkB signaling by removal of one BDNF allele could be partially rescued by TrkB.T1 deletion, which was revealed by an amelioration of the enhanced aggression and weight gain associated with BDNF haploinsufficiency. Our results suggest that, at the physiological level, TrkB.T1 receptors are important regulators of TrkB.FL signaling in vivo. Moreover, TrkB.T1 selectively affects dendrite complexity of certain neuronal populations.

Key words: TrkB.T1; BDNF; mouse; anxiety; neurites; amygdala

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Received Oct. 20, 2008; revised Dec. 5, 2008; accepted Dec. 10, 2008.

Correspondence should be addressed to Dr. Lino Tessarollo, Neural Development Group, Mouse Cancer Genetics Program, National Cancer Institute–Frederick, 7th Street, Building 560, Room 32-31D, P.O. Box B, Frederick, MD 21702. Email: tessarol{at}mail.nih.gov

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