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J Neurosci. 2014 Mar 5;34(10):3517-22. doi: 10.1523/JNEUROSCI.2955-13.2014.

Aberrant development and plasticity of excitatory visual cortical networks in the absence of cpg15.

Author information

1
F.M. Kirby Neurobiology Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, and Picower Institute for Learning and Memory, Department of Biology, Harvard-MIT Division of Health Science and Technology, and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139.

Abstract

During development, experience plays a crucial role in sculpting neuronal connections. Patterned neural activity guides formation of functional neural circuits through the selective stabilization of some synapses and the pruning of others. Activity-regulated factors are fundamental to this process, but their roles in synapse stabilization and maturation is still poorly understood. CPG15, encoded by the activity-regulated gene candidate plasticity gene 15, is a small, glycosylphosphatidylinositol (GPI)-linked, extracellular protein that promotes synapse stabilization. Here we show that global knock-out of cpg15 results in abnormal postnatal development of the excitatory network in visual cortex and an associated disruption in development of visual receptive field properties. In addition, whereas repeated stimulation induced potentiation and depression in wild-type mice, the depression was slower in cpg15 knock-out mice, suggesting impairment in short-term depression-like mechanisms. These findings establish the requirement for cpg15 in activity-dependent development of the visual system and demonstrate the importance of timely excitatory network development for normal visual function.

KEYWORDS:

depression; plasticity; potentiation; visual cortex

PMID:
24599452
PMCID:
PMC3942571
DOI:
10.1523/JNEUROSCI.2955-13.2014
[Indexed for MEDLINE]
Free PMC Article

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