Dominick P. Purpura Department of Neuroscience Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Cold Spring Harb Perspect Biol. 2012 Feb 1;4(2):a005728. doi: 10.1101/cshperspect.a005728.
Ubiquitous forms of long-term potentiation (LTP) and depression (LTD) are caused by enduring increases or decreases in neurotransmitter release. Such forms or presynaptic plasticity are equally observed at excitatory and inhibitory synapses and the list of locations expressing presynaptic LTP and LTD continues to grow. In addition to the mechanistically distinct forms of postsynaptic plasticity, presynaptic plasticity offers a powerful means to modify neural circuits. A wide range of induction mechanisms has been identified, some of which occur entirely in the presynaptic terminal, whereas others require retrograde signaling from the postsynaptic to presynaptic terminals. In spite of this diversity of induction mechanisms, some common induction rules can be identified across synapses. Although the precise molecular mechanism underlying long-term changes in transmitter release in most cases remains unclear, increasing evidence indicates that presynaptic LTP and LTD can occur in vivo and likely mediate some forms of learning.
普遍存在的长时程增强(LTP)和长时程抑制(LTD)是由神经递质释放的持久增加或减少引起的。这种形式的或突触前可塑性在兴奋性和抑制性突触上同样被观察到,并且表达突触前 LTP 和 LTD 的位置列表不断增加。除了在机制上不同的突触后可塑性形式外,突触前可塑性提供了一种强大的方式来修饰神经回路。已经确定了广泛的诱导机制,其中一些完全发生在突触前末端,而另一些则需要从突触后到突触前末端的逆行信号。尽管存在这种多样性的诱导机制,但可以在不同的突触之间识别出一些共同的诱导规则。尽管在大多数情况下,导致递质释放的长期变化的确切分子机制仍不清楚,但越来越多的证据表明,突触前 LTP 和 LTD 可以在体内发生,并可能介导某些形式的学习。