García-Junco-Clemente P, Linares-Clemente P, Fernández-Chacón R
Departamento de Fisiología Médica y Biofísica, Facultad de Medicina, Universidad de Sevilla. Avda. Sánchez-Pizjuán 4, Sevilla, Spain.
Mol Psychiatry. 2005 Feb;10(2):185-200; image 131. doi: 10.1038/sj.mp.4001628.
Some of the most abundant synapses in the brain such as the synapses formed by the hippocampal mossy fibers, cerebellar parallel fibers and several types of cortical afferents express presynaptic forms of long-term potentiation (LTP), a putative cellular model for spatial, motor and fear learning. Those synapses often display presynaptic mechanisms of LTP induction, which are either NMDA receptor independent of dependent of presynaptic NMDA receptors. Recent investigations on the molecular mechanisms of neurotransmitter release modulation in short- and long-term synaptic plasticity in central synapses give a preponderant role to active zone proteins as Munc-13 and RIM1-alpha, and point toward the maturation process of synaptic vesicles prior to Ca(2+)-dependent fusion as a key regulatory step of presynaptic plasticity.
大脑中一些最为丰富的突触，比如由海马苔藓纤维、小脑平行纤维以及几种类型的皮质传入纤维所形成的突触，表达突触前形式的长时程增强（LTP），这是一种用于空间、运动和恐惧学习的假定细胞模型。这些突触常常展现出LTP诱导的突触前机制，其要么独立于NMDA受体，要么依赖于突触前NMDA受体。近期关于中枢突触短期和长期突触可塑性中神经递质释放调节分子机制的研究表明，诸如Munc-13和RIM1-α等活性区蛋白发挥着主要作用，并指出在Ca(2+)依赖性融合之前突触小泡的成熟过程是突触前可塑性的关键调节步骤。
