The protein kinase C phosphorylation site on GAP-43 differentially regulates information storage.
Protein kinase C (PKC) is known to regulate phosphorylation of substrates such as MARCKS, GAP-43, and the NMDA receptor, all of which have been linked to synaptic plasticity underlying information storage processes. Here we report on three transgenic mice isoforms differentiated both by mutation of the PKC site on GAP-43 as well as by their performance in three learning situations: (1) a radial arm maze task, which evaluates spatial memory and its retention, (2) fear conditioning which assesses contextual memory, and (3) the water maze which also evaluates spatial memory and its retention. The present results show, for the first time to our knowledge, that the phosphorylation state of a single site on an identified brain growth- and plasticity-associated protein differentially regulates performance of three different memory-associated tasks.
Holahan
Matthew
M
Department of Psychology and Institute of Neuroscience, Carleton University, Ottawa, Canada. matthew_holahan@carleton.ca
Routtenberg
Aryeh
A
D000818:Animals; D001921:Brain / Q000378:metabolism*; D019922:GAP-43 Protein / Q000235:genetics / Q000378:metabolism*; D007858:Learning / Q000502:physiology*; D008568:Memory / Q000502:physiology*; D051379:Mice; D008822:Mice, Transgenic; D009473:Neuronal Plasticity / Q000502:physiology*; D010766:Phosphorylation; D020033:Protein Isoforms; D011493:Protein Kinase C / Q000378:metabolism*
D019922:GAP-43 Protein; D020033:Protein Isoforms; D011493:Protein Kinase C