Chevaleyre Vivien, Takahashi Kanji A, Castillo Pablo E
Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Annu Rev Neurosci. 2006;29:37-76. doi: 10.1146/annurev.neuro.29.051605.112834.
Changes in synaptic efficacy are thought to be crucial to experience-dependent modifications of neural function. The diversity of mechanisms underlying these changes is far greater than previously expected. In the last five years, a new class of use-dependent synaptic plasticity that requires retrograde signaling by endocannabinoids (eCB) and presynaptic CB1 receptor activation has been identified in several brain structures. eCB-mediated plasticity encompasses many forms of transient and long-lasting synaptic depression and is found at both excitatory and inhibitory synapses. In addition, eCBs can modify the inducibility of non-eCB-mediated forms of plasticity. Thus, the eCB system is emerging as a major player in synaptic plasticity. Given the wide distribution of CB1 receptors in the CNS, the list of brain structures and synapses expressing eCB-mediated plasticity is likely to expand.
突触效能的变化被认为对于神经功能的经验依赖性修饰至关重要。这些变化背后的机制多样性远比之前预期的要大得多。在过去五年中，一类新的依赖使用的突触可塑性已在多个脑结构中被发现，这类可塑性需要内源性大麻素（eCB）进行逆行信号传递以及突触前CB1受体激活。eCB介导的可塑性包括多种形式的短暂和持久突触抑制，并且在兴奋性和抑制性突触中均有发现。此外，eCB可以改变非eCB介导的可塑性形式的诱导性。因此，eCB系统正成为突触可塑性中的一个主要参与者。鉴于CB1受体在中枢神经系统中广泛分布，表达eCB介导可塑性的脑结构和突触的清单可能会扩大。
