MODIFIED HIPPOCAMPAL LONG-TERM POTENTIATION IN PKC-GAMMA-MUTANT MICE.
1253 - 1262.
Calcium-phospholipid-dependent protein kinase (PKC) has long been suggested to play an important role in modulating synaptic efficacy. We have created a strain of mice that lacks the gamma subtype of PKC to evaluate the significance of this brain-specific PKC isozyme in synaptic plasticity. Mutant mice are viable, develop normally, and have synaptic transmission that is indistinguishable from wild-type mice. Long-term potentiation (LTP), however, is greatly diminished in mutant animals, while two other forms of synaptic plasticity, long-term depression and paired-pulse facilitation, are normal. Surprisingly, when tetanus to evoke LTP was preceded by a low frequency stimulation, mutant animals displayed apparently normal LTP. We propose that PKCgamma is not part of the molecular machinery that produces LTP but is a key regulatory component.
|Title:||MODIFIED HIPPOCAMPAL LONG-TERM POTENTIATION IN PKC-GAMMA-MUTANT MICE|
|Keywords:||PROTEIN-KINASE-C, INDUCTION, EXPRESSION, CALMODULIN, LTP, CA1, TRANSMISSION, MAINTENANCE, ACTIVATION, CURRENTS|
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