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GAP-43 in synaptic plasticity: molecular perspectives

Authors Holahan MR

Received 20 March 2015

Accepted for publication 1 May 2015

Published 18 June 2015 Volume 2015:5 Pages 137—146

DOI https://doi.org/10.2147/RRBC.S73846

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Professor Nikolay Dokholyan

Matthew R Holahan

Department of Neuroscience, Carleton University, Ottawa, ON, Canada

Abstract:
The growth-associated protein, GAP-43 (also known as F1, neuromodulin, B-50), participates in the developmental regulation of axonal growth and neural network formation via protein kinase C-mediated regulation of cytoskeletal elements. Transgenic overexpression of GAP-43 can result in the formation of new synapses, neurite outgrowth, and synaptogenesis after injury. In a number of adult mammalian species, GAP-43 has been implicated in the regulation of synaptic transmission and plasticity, such as long-term potentiation, drug sensitization, and changes in memory processes. This review examines the molecular and biochemical attributes of GAP-43, its distribution in the central nervous system, subcellular localization, role in neurite outgrowth and development, and functions related to plasticity, such as those occurring during long-term potentiation, memory formation, and drug sensitization.

Keywords:
GAP-43, protein kinase C, axons, development, regeneration, long-term potentiation, memory

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