Helmholtz Gemeinschaft


Impaired synapse function during postnatal development in the absence of CALEB, an EGF-like protein processed by neuronal activity

Official URL:https://doi.org/10.1016/j.neuron.2005.02.027
PubMed:View item in PubMed
Creators Name:Juettner, R. and More, M.I. and Das, D. and Babich, A. and Meier, J. and Henning, M. and Erdmann, B. and Mueller, E.C. and Otto, A. and Grantyn, R. and Rathjen, F.G.
Journal Title:Neuron
Journal Abbreviation:Neuron
Page Range:233-245
Date:21 May 2005
Keywords:Amino Acid Sequence, Western Blotting, Epidermal Growth Factor, Excitatory Postsynaptic Potentials, Immunohistochemistry, Membrane Glycoproteins, Knockout Mice, Electron Transmission Microscopy, Molecular Sequence Data, Nerve Tissue Proteins, Organ Culture Techniques, Superior Colliculi, Synapses, Animals, Chick Embryo
Abstract:In an attempt to characterize the molecular components by which electric activity influences the development of synapses, we searched for cell surface proteins modulated by calcium influx and glutamate receptor activity. Here, we report that neuronal depolarization facilitates the conversion of CALEB, which results in a truncated transmembrane form with an exposed EGF domain. To characterize the role of CALEB in synapse development, synaptic features were investigated in slices of the colliculus superior from CALEB-deficient mice. In the absence of CALEB, the number of synapses and their morphological characteristics remained unchanged. However, in CALEB-deficient mice, synapses displayed higher paired-pulse ratios, less depression during prolonged repetitive activation, a lower rate of spontaneous postsynaptic currents, and a lower release probability at early but not mature postnatal stages. Our findings indicate that CALEB provides a molecular basis for maintaining normal release probability at early developmental stages.
Publisher:Cell Press (U.S.A.)
Additional Information:The original publication is available at www.sciencedirect.com
Item Type:Article

Repository Staff Only: item control page

Open Access
MDC Library