Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.mcn.2013.12.004
Title: Gαz regulates BDNF-induction of axon growth in cortical neurons
Authors: Hultman, R.
Kumari, U.
Michel, N.
Casey, P.J. 
Keywords: BDNF
G proteins
GNAZ
Neurotrophin
Issue Date: Jan-2014
Citation: Hultman, R., Kumari, U., Michel, N., Casey, P.J. (2014-01). Gαz regulates BDNF-induction of axon growth in cortical neurons. Molecular and Cellular Neuroscience 58 : 53-61. ScholarBank@NUS Repository. https://doi.org/10.1016/j.mcn.2013.12.004
Abstract: The disruption of neurotransmitter and neurotrophic factor signaling in the central nervous system (CNS) is implicated as the root cause of neuropsychiatric disorders, including schizophrenia, epilepsy, chronic pain, and depression. Therefore, identifying the underlying molecular mechanisms by which neurotransmitter and neurotrophic factor signaling regulates neuronal survival or growth may facilitate identification of more effective therapies for these disorders. Previously, our lab found that the heterotrimeric G protein, Gz, mediates crosstalk between G protein-coupled receptors and neurotrophin signaling in the neural cell line PC12. These data, combined with Gαz expression profiles - predominantly in neuronal cells with higher expression levels corresponding to developmental times of target tissue innervation - suggested that Gαz may play an important role in neurotrophin signaling and neuronal development. Here, we provide evidence in cortical neurons, both manipulated ex vivo and those cultured from Gz knockout mice, that Gαz is localized to axonal growth cones and plays a significant role in the development of axons of cortical neurons in the CNS. Our findings indicate that Gαz inhibits BDNF-stimulated axon growth in cortical neurons, establishing an endogenous role for Gαz in regulating neurotrophin signaling in the CNS. © 2013 Elsevier Inc.
Source Title: Molecular and Cellular Neuroscience
URI: http://scholarbank.nus.edu.sg/handle/10635/110104
ISSN: 10447431
DOI: 10.1016/j.mcn.2013.12.004
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