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Metaplasticity governs compartmentalization of synaptic tagging and capture through brain-derived neurotrophic
 

Summary: Metaplasticity governs compartmentalization of synaptic
tagging and capture through brain-derived neurotrophic
factor (BDNF) and protein kinase M (PKM)
Sreedharan Sajikumar and Martin Korte1
Zoological Institute, Division of Cellular Neurobiology, TU Braunschweig, D-38106 Braunschweig, Germany
Edited by Mu-ming Poo, University of California, Berkeley, CA, and approved December 27, 2010 (received for review November 11, 2010)
Activity-dependent synaptic plasticity is widely accepted to be the
cellular correlate of learning and memory. It is believed that
associativity between different synaptic inputs can transform
short-lasting forms of synaptic plasticity (<3 h) to long-lasting
ones. Synaptic tagging and capture (STC) might be able to explain
this heterosynaptic support, because it distinguishes between lo-
cal mechanisms of synaptic tags and cell-wide mechanisms respon-
sible for the synthesis of plasticity-related proteins (PRPs). STC
initiate storage processes only when the strength of the synaptic
tag and the local concentration of essential proteins are above
a certain plasticity threshold. We present evidence that priming
stimulation through the activation of metabotropic glutamate
receptors substantially increases the "range of threshold" for func-
tional plasticity by producing protein kinase M (PKM) as a PRP

  

Source: Alford, Simon - Department of Biological Sciences, University of Illinois at Chicago

 

Collections: Biology and Medicine