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Phosphorylation of CREB and DARPP‐32 during late LTP at hippocampal to prefrontal cortex synapses in vivo
Author(s) -
Hotte Maïté,
Thuault Sébastien,
Dineley Kelly T.,
Hemmings Hugh C.,
Nairn Angus C.,
Jay Thérèse M.
Publication year - 2007
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.20339
Subject(s) - long term potentiation , neuroscience , creb , prefrontal cortex , hippocampal formation , hippocampus , postsynaptic potential , synapse , nmda receptor , neuronal memory allocation , chemistry , phosphorylation , biology , metaplasticity , microbiology and biotechnology , receptor , biochemistry , transcription factor , cognition , gene
Abstract Specific patterns of stimulation applied in the ventral hippocampus produce long‐term potentiation (LTP) of postsynaptic synapses in the prefrontal cortex in vivo. The induction of LTP is dependent on NMDA receptors and cAMP‐dependant kinase (PKA) activation. Yet little is known concerning the cellular mechanisms underlying the expression of this neocortical form of LTP. In the present study, we tested whether LTP at hippocampal to prefrontal cortex synapses leads to activation of DARPP‐32 and CREB as well as defined the temporal regulation of the phosphorylation states of both proteins. Our data indicate a peak in CREB and DARPP‐32 phosphorylation during the late phase of prefrontal LTP (2 h posttetanus). These findings support the hypothesis that prolonged expression of hippocampal‐prefrontal cortex LTP depends on a synergistic mechanism involving phosphorylation of both CREB and DARPP‐32 via activation of the cAMP/PKA‐dependent pathway. Synapse 61:24–28, 2007. © 2006 Wiley‐Liss, Inc.