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SNAP‐25 requirement for dendritic growth of hippocampal neurons
Author(s) -
Grosse Gisela,
Grosse Johannes,
Tapp Rosemarie,
Kuchinke Jörg,
Gorsleben Martin,
Fetter Ingmar,
HöhneZell Barbara,
Gratzl Manfred,
Bergmann Mathias
Publication year - 1999
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19990601)56:5<539::aid-jnr9>3.0.co;2-y
Subject(s) - synaptobrevin , hippocampal formation , microbiology and biotechnology , exocytosis , neuroscience , dendrite (mathematics) , biology , transferrin receptor , chemistry , synaptic vesicle , receptor , vesicle , biochemistry , secretion , geometry , mathematics , membrane
Structure and dimension of the dendritic arbor are important determinants of information processing by the nerve cell, but mechanisms and molecules involved in dendritic growth are essentially unknown. We investigated early mechanisms of dendritic growth using mouse fetal hippocampal neurons in primary culture, which form processes during the first week in vitro. We detected a key component of regulated exocytosis, SNAP‐25 (synaptosomal associated protein of 25 kDa), in axons and axonal terminals as well as in dendrites identified by the occurrence of the dendritic markers transferrin receptor and MAP2. Selective inactivation of SNAP‐25 by botulinum neurotoxin A (BoNTA) resulted in inhibition of axonal growth and of vesicle recycling in axonal terminals. In addition, dendritic growth of hippocampal pyramidal and granule neurons was significantly inhibited by BoNTA. In contrast, cleavage of synaptobrevin by tetanus toxin had an effect on neither axonal nor dendritic growth. Our observations indicate that SNAP‐25, but not synaptobrevin, is involved in constitutive axonal growth and dendrite formation by hippocampal neurons. J. Neurosci. Res. 56:539–546, 1999. © 1999 Wiley‐Liss, Inc.