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Molecular Pharmacology Fast Forward
First published on July 26, 2005; DOI: 10.1124/mol.105.017277

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Received for publication July 26, 2005.
Revised July 25, 2005.
Accepted for publication July 26, 2005.

NGF requirement for neuronal survival? NO thanks! (Relates to Article by Culmsee, et al. FastForward 18 July 2005)

Katerina Akassoglou 1*

1 University of California, San Diego

* Address correspondence to: E-mail: aakasoglou{at}ucsd.edu

Abstract

Due to the limited therapeutic applications of Nerve Growth Factor (NGF), there has been increasing focus on the development of pharmacological tools to bypass the requirement of NGF for the activation of the TrkA tyrosine kinase receptor neuronal survival pathway. In this issue of Molecular Pharmacology, the work by Culmsee et al. shows that NGF-independent activation of TrkA by protein tyrosine phosphatase (PTP) inhibitors is only achieved when accompanied by release of nitric oxide (NO). This work identifies the integration of the NO/cGMP/PKG and the NGF/TrkA pathways to induce activation of Akt and ERK1/2 and mediate neuronal survival in the absence of NGF. In addition, it underscores the potential therapeutic effects of Ethyl-3,4-dephostatin (DPN), a stable analogue of the naturally occurring PTP inhibitor dephostatin, that serves as a NO-donor and protects neurons from apoptosis. This perspective comparatively reviews two major signal transduction pathways that mediate NGF-independent neuronal survival by activating the TrkA pathway: the NO/cGMP/PKG and adenosine/G-protein coupled receptor (GPCR) pathways.


Key words: Adenosine, NGF/EGF, Guanylyl cyclase, Nitric oxide, Nitric oxide synthases, Protein Kinase G, Excitotoxicity, neurodegeneration


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