The regulation of dendritic arbor development and plasticity by glutamatergic synaptic input: a review of the synaptotrophic hypothesis

Cline, H. T., Haas, K. (March 2008) The regulation of dendritic arbor development and plasticity by glutamatergic synaptic input: a review of the synaptotrophic hypothesis. J Physiol, 586 (6). pp. 1509-1517.

Abstract

Abstract: The synaptotropic hypothesis, which states that synaptic inputs control the elaboration of dendritic (and axonal) arbors was articulated by Vaughn in 1989. Today the role of synaptic inputs in controlling neuronal structural development remains an area of intense research activity. Several recent studies have applied modern molecular genetic, imaging and electrophysiological methods to this question and now provide strong evidence that maturation of excitatory synaptic inputs is required for the development of neuronal structure in the intact brain. Here we critically review data concerning the hypothesis with the expectation that understanding the circumstances when the data do and do not support the hypothesis will be most valuable. The synaptotrophic hypothesis contributes at both conceptual and mechanistic levels to our understanding of how relatively minor changes in levels or function of synaptic proteins may have profound effects on circuit development and plasticity.

Item Type: Paper
Uncontrolled Keywords: Dendrite Plasticity Synaptic transmission
Subjects: Investigative techniques and equipment > imaging
organs, tissues, organelles, cell types and functions > cell types and functions > cell types > neurons
organs, tissues, organelles, cell types and functions > cell types and functions > cell types > neurons
organs, tissues, organelles, cell types and functions > cell types and functions > cell types > neurons
CSHL Authors:
Communities: CSHL labs > Cline lab
Depositing User: Tom Adams
Date: 15 March 2008
Date Deposited: 25 Aug 2011 18:36
Last Modified: 13 Mar 2018 20:33
PMCID: PMC2375708
Related URLs:
URI: https://repository.cshl.edu/id/eprint/7711

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