Presynaptic LTP and LTD of excitatory and inhibitory synapses

Abstract

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.

Figure 1.

Four basic arrangements for presynaptic LTP and LTD. (Top row) Illustrates examples where plasticity is entirely induced presynaptically, either in a homosynaptically (e.g., mossy fiber LTP) or heterosynaptically (e.g., associative cortico-lateral amygdala LTP of glutamatergic transmission). (Bottom row) Examples requiring retrograde signaling generated either at the same synapse receiving the signal (left, e.g., eCB-LTD at excitatory synapses) or at a neighboring synapse (right, e.g., eCB-LTD at inhibitory synapses).

Figure 2.

Expression mechanisms of presynaptic LTP and LTD: three prototypical examples (see text).