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Activation of a K‐252b‐Sensitive Protein Kinase is Necessary for a Post‐Synaptic Phase of Long‐Term Potentiation in Area CA1 of Rat Hippocampus
Author(s) -
Reymann K. G.,
Davies S. N.,
Matthies H.,
Kase H.,
Collingridge G. L.
Publication year - 1990
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1990.tb00439.x
Subject(s) - long term potentiation , hippocampus , neuroscience , term (time) , synaptic plasticity , chemistry , biophysics , biology , biochemistry , physics , receptor , quantum mechanics
K‐252b, a potent inhibitor of protein kinases blocked a late phase of long‐term potentiation (LTP) in area CA1 of rat hippocampal slices, resulting in decremental LTP. It also prevented the slowly developing increase in sensitivity of CA1 neurons to iontophoretically administered α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA) which was seen in control slices that exhibit nondecremental LTP. However, K‐252b applied 60–180 min after the induction of LTP had no effect on the potentiated synaptic and AMPA‐induced responses. A K‐252b‐sensitive protein kinase may therefore be involved in a slowly developing postsynaptic component of LTP.