Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
The Biotechnology Centre of Oslo, University of Oslo, Forskningsparken, Gaustadalléen 21, 0349 Oslo, Norway.
Neuron. 2014 May 21;82(4):859-71. doi: 10.1016/j.neuron.2014.04.003. Epub 2014 May 1.
Posttetanic potentiation (PTP) is a widely observed form of short-term plasticity lasting for tens of seconds after high-frequency stimulation. Here we show that although protein kinase C (PKC) mediates PTP at the calyx of Held synapse in the auditory brainstem before and after hearing onset, PTP is produced primarily by an increased probability of release (p) before hearing onset, and by an increased readily releasable pool of vesicles (RRP) thereafter. We find that these mechanistic differences, which have distinct functional consequences, reflect unexpected differential actions of closely related calcium-dependent PKC isoforms. Prior to hearing onset, when PKCγ and PKCβ are both present, PKCγ mediates PTP by increasing p and partially suppressing PKCβ actions. After hearing onset, PKCγ is absent and PKCβ produces PTP by increasing RRP. In hearing animals, virally expressed PKCγ overrides PKCβ to produce PTP by increasing p. Thus, two similar PKC isoforms mediate PTP in distinctly different ways.
强直后增强（PTP）是一种广泛存在的短期可塑性形式，在高频刺激后持续数十秒。在这里，我们表明，尽管蛋白激酶 C（PKC）在听觉脑干中的 Held 突触前叶在听觉开始前后介导 PTP，但 PTP 主要是通过听觉开始前释放概率（p）的增加以及此后易释放囊泡（RRP）池的增加产生的。我们发现，这些具有不同功能后果的机制差异反映了密切相关的钙依赖性 PKC 同工型的意外差异作用。在听觉开始之前，当 PKCγ 和 PKCβ 都存在时，PKCγ 通过增加 p 并部分抑制 PKCβ 的作用来介导 PTP。听觉开始后，PKCγ 不存在，PKCβ 通过增加 RRP 产生 PTP。在听觉动物中，病毒表达的 PKCγ 通过增加 p 来取代 PKCβ 产生 PTP。因此，两种相似的 PKC 同工型以截然不同的方式介导 PTP。
