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Endogenous protein kinase A inhibitor (PKIα) modulates synaptic activity
Author(s) -
de Lecea Luis,
Criado José R.,
Rivera Santiago,
Wen Wei,
Soriano Eduardo,
Henriksen Steven J.,
Taylor Susan S.,
Gall Christine M.,
Sutcliffe J. Gregor
Publication year - 1998
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19980801)53:3<269::aid-jnr1>3.0.co;2-8
Subject(s) - long term potentiation , synaptic plasticity , protein kinase a , neuroscience , endogeny , signal transduction , microbiology and biotechnology , chemistry , stimulation , biology , kinase , biochemistry , receptor
Protein kinase A (PKA) has long been known to be involved in major regulatory mechanisms underlying synaptic plasticity and complex behaviors such as learning and memory. The endogenous PKA inhibitor, PKIα, has been extensively studied for its effects on PKA and PKA‐mediated signal transduction. Clear functions for PKIα in vivo, however, remain to be established. Here we describe that several forms of synaptic stimulation in the rat hippocampus cause a dramatic decrease in the concentration of PKIα in dentate granule cells. Furthermore, chronic infusion of antisense oligonucleotides against PKIα into the rat brain results in a dramatic reduction of the excitability of these neurons and elimination of their ability to exhibit long‐term potentiation (LTP) and long‐term depression (LTD), suggesting a stimulus‐dependent regulatory role for PKIα in PKA signal transduction. J. Neurosci. Res. 53:269–278, 1998. © 1998 Wiley‐Liss, Inc.