Modified hippocampal long-term potentiation in PKC gamma-mutant mice.
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 PKC gamma is not part of the molecular machinery that produces LTP but is a key regulatory component.
Abeliovich
A
A
Howard Hughes Medical Institute, Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.
Chen
C
C
Goda
Y
Y
Silva
A J
AJ
Stevens
C F
CF
Tonegawa
S
S
D000818:Animals; D001483:Base Sequence; D017931:DNA Primers / Q000737:chemistry; D006624:Hippocampus / Q000502:physiology*; D015640:Ion Channel Gating; D017774:Long-Term Potentiation; D008564:Membrane Potentials; D051379:Mice; D018345:Mice, Knockout; D008969:Molecular Sequence Data; D009473:Neuronal Plasticity; D011493:Protein Kinase C / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology; D009435:Synaptic Transmission
D017931:DNA Primers; D016194:Receptors, N-Methyl-D-Aspartate; D011493:Protein Kinase C