MODIFIED HIPPOCAMPAL LONG-TERM POTENTIATION IN PKC-GAMMA-MUTANT MICE
MODIFIED HIPPOCAMPAL LONG-TERM POTENTIATION IN PKC-GAMMA-MUTANT MICE
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DOI：
10.1016/0092-8674(93)90613-u
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发表时间：
1993-12-31
期刊：
影响因子：
64.5
通讯作者：
TONEGAWA, S
中科院分区：
文献类型：
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作者：
ABELIOVICH, A;CHEN, C;TONEGAWA, S
钙磷脂依赖性蛋白激酶（PKC）一直被认为在调节突触效能中起重要作用。我们建立了一种缺乏PKC γ亚型的小鼠品系，以评估这种脑特异性PKC同工酶在突触可塑性中的意义。突变小鼠是可行的，正常发育，并具有与野生型小鼠无法区分的突触传递。然而，长时程增强（LTP）在突变动物中大大减少，而其他两种形式的突触可塑性，长时程抑制和成对脉冲易化，是正常的。令人惊讶的是，当破伤风诱发LTP之前的低频刺激，突变动物表现出明显正常的LTP。我们认为PKC γ不是产生LTP的分子机制的一部分，而是一个关键的调控成分。
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.