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MODIFIED HIPPOCAMPAL LONG-TERM POTENTIATION IN PKC-GAMMA-MUTANT MICE

ABELIOVICH, A; CHEN, C; GODA, Y; SILVA, AJ; STEVENS, CF; TONEGAWA, S; (1993) MODIFIED HIPPOCAMPAL LONG-TERM POTENTIATION IN PKC-GAMMA-MUTANT MICE. CELL , 75 (7) 1253 - 1262.

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Abstract

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.

Type:Article
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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