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Post-Lesion Neural Plasticity pp 93–101Cite as

Protein Kinase C and Protein F1: Potential Molecular Mediators of Lesion-Induced Synaptic Plasticity Recapitulate Developmental Plasticity

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Abstract

This review is focused on the suggestion that a potential molecular mechanism involving protein kinase C and its substrate protein F1 may be directly involved in the process of mediating lesion-induced neuronal plasticity. As several chapters in this Volume illustrate, after damage to the nervous system, intact neurons show growth activities such as axonal sprouting. Under certain conditions this can lead to recovery of function, in whole or in part. The mechanisms for this process are not known, though some recent clues from biochemistry suggest particular proteins that may be essential for the process. In this review I wish to emphasize one essential point: that the input-dependent molecular mechanism related to synaptic growth of intact synapses is also recruited by injury-produced growth factors that stimulate the response to nerve injury.

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Author information

Authors and Affiliations

  1. Cresap Neuroscience Laboratory, Northwestern University, Evanston, IL, 60201, USA

    A. Routtenberg

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  1. A. Routtenberg
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Editors and Affiliations

  1. Dept. of Neurobiology, University of Bremen, NW2, Postfach 330440, D-2800, Bremen 33, Federal Republic of Germany

    Hans Flohr

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© 1988 Springer-Verlag Berlin Heidelberg

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Routtenberg, A. (1988). Protein Kinase C and Protein F1: Potential Molecular Mediators of Lesion-Induced Synaptic Plasticity Recapitulate Developmental Plasticity. In: Flohr, H. (eds) Post-Lesion Neural Plasticity. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73849-4_9

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  • DOI: https://doi.org/10.1007/978-3-642-73849-4_9

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-73851-7

  • Online ISBN: 978-3-642-73849-4

  • eBook Packages: Springer Book Archive

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