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Phosphorylation of proteins involved in activity‐dependent forms of synaptic plasticity is altered in hippocampal slices maintained in vitro
Author(s) -
Ho Oanh H.,
Delgado Jary Y.,
O'Dell Thomas J.
Publication year - 2004
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2004.02815.x
Subject(s) - long term potentiation , synaptic plasticity , ampa receptor , phosphorylation , microbiology and biotechnology , nmda receptor , biology , kinase , hippocampal formation , protein kinase a , glutamate receptor , neuroscience , biochemistry , receptor
The acute hippocampal slice preparation has been widely used to study the cellular mechanisms underlying activity‐dependent forms of synaptic plasticity such as long‐term potentiation (LTP) and long‐term depression (LTD). Although protein phosphorylation has a key role in LTP and LTD, little is known about how protein phosphorylation might be altered in hippocampal slices maintained in vitro . To begin to address this issue, we examined the effects of slicing and in vitro maintenance on phosphorylation of six proteins involved in LTP and/or LTD. We found that AMPA receptor (AMPAR) glutamate receptor 1 (GluR1) subunits are persistently dephosphorylated in slices maintained in vitro for up to 8 h. α calcium/calmodulin‐dependent kinase II (αCamKII) was also strongly dephosphorylated during the first 3 h in vitro but thereafter recovered to near control levels. In contrast, phosphorylation of the extracellular signal‐regulated kinase ERK2, the ERK kinase MEK, proline‐rich tyrosine kinase 2 (Pyk2), and Src family kinases was significantly, but transiently, increased. Electrophysiological experiments revealed that the induction of LTD by low‐frequency synaptic stimulation was sensitive to time in vitro . These findings indicate that phosphorylation of proteins involved in N ‐methyl‐ d ‐aspartate (NMDA) receptor‐dependent forms of synaptic plasticity is altered in hippocampal slices and suggest that some of these changes can significantly influence the induction of LTD.