Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461, USA; email:
Department of Neuroscience, Physiology and Pharmacology, University College London, London WC1E 6BT, United Kingdom.
Annu Rev Neurosci. 2018 Jul 8;41:299-322. doi: 10.1146/annurev-neuro-080317-062155. Epub 2018 Apr 25.
Long-lasting changes of brain function in response to experience rely on diverse forms of activity-dependent synaptic plasticity. Chief among them are long-term potentiation and long-term depression of neurotransmitter release, which are widely expressed by excitatory and inhibitory synapses throughout the central nervous system and can dynamically regulate information flow in neural circuits. This review article explores recent advances in presynaptic long-term plasticity mechanisms and contributions to circuit function. Growing evidence indicates that presynaptic plasticity may involve structural changes, presynaptic protein synthesis, and transsynaptic signaling. Presynaptic long-term plasticity can alter the short-term dynamics of neurotransmitter release, thereby contributing to circuit computations such as novelty detection, modifications of the excitatory/inhibitory balance, and sensory adaptation. In addition, presynaptic long-term plasticity underlies forms of learning and its dysregulation participates in several neuropsychiatric conditions, including schizophrenia, autism, intellectual disabilities, neurodegenerative diseases, and drug abuse.
长期以来，大脑功能的变化依赖于多种形式的活动依赖性突触可塑性。其中主要包括神经递质释放的长时程增强和长时程抑制，它们广泛存在于中枢神经系统的兴奋性和抑制性突触中，可以动态调节神经回路中的信息流。本文综述了突触前长时程可塑性机制的最新进展及其对回路功能的贡献。越来越多的证据表明，突触前可塑性可能涉及结构变化、突触前蛋白合成和突触间信号转导。突触前长时程可塑性可以改变神经递质释放的短期动力学，从而有助于新奇检测、兴奋性/抑制性平衡的调节以及感觉适应等电路计算。此外，突触前长时程可塑性是学习的基础，其失调参与了多种神经精神疾病，包括精神分裂症、自闭症、智力障碍、神经退行性疾病和药物滥用。
