Huang Y Y, Colino A, Selig D K, Malenka R C
Department of Psychiatry, University of California, San Francisco 94143.
Science. 1992 Feb 7;255(5045):730-3. doi: 10.1126/science.1346729.
Long-term potentiation (LTP) is an extensively studied model of synaptic plasticity, in part because it is a plausible biological correlate for the Hebbian synaptic modification that forms the basis for theoretical models of neural development, learning, and memory. Although these models must incorporate algorithms that constrain synaptic weight changes, physiological evidence for such mechanisms is limited. Examination of LTP in area CA1 of the hippocampus revealed that the threshold for LTP induction was not fixed but could be strongly influenced by the recent history of synaptic activity. This effect was transient, synapse-specific, and dependent on postsynaptic N-methyl-D-aspartate (NMDA) receptor activation. These results suggest that the threshold for LTP induction may be continually adjusted according to the recent history of NMDA receptor activation and provide a physiological mechanism by which LTP can be transiently inhibited.
长时程增强(LTP)是一种经过广泛研究的突触可塑性模型,部分原因在于它是赫布式突触修饰的一种合理生物学关联,而赫布式突触修饰构成了神经发育、学习和记忆理论模型的基础。尽管这些模型必须纳入限制突触权重变化的算法,但此类机制的生理学证据有限。对海马体CA1区LTP的研究表明,LTP诱导的阈值并非固定不变,而是会受到突触活动近期历史的强烈影响。这种效应是短暂的、突触特异性的,且依赖于突触后N-甲基-D-天冬氨酸(NMDA)受体的激活。这些结果表明,LTP诱导的阈值可能会根据NMDA受体激活的近期历史不断调整,并提供了一种可短暂抑制LTP的生理机制。