Fitzjohn S M, Pickard L, Duckworth J K, Molnar E, Henley J M, Collingridge G L, Noël J
MRC Centre for Synaptic Plasticity, Department of Anatomy, University of Bristol, School of Medical Sciences, University Walk, BS8 1TD, Bristol, UK.
Neuropharmacology. 2001 Nov;41(6):693-9. doi: 10.1016/s0028-3908(01)00128-9.
Long-term potentiation (LTP) of synaptic transmission is under intense investigation. It is believed that the mechanisms involved in its induction and expression are critically involved in synaptic processes that are important for learning and memory and other physiological functions. A reliable means of inducing LTP in dissociated cultured neurones would facilitate investigations into the molecular basis of LTP but has been hard to achieve. Here we report a mechanism for inducing LTP in postnatal dissociated hippocampal neurones using transient depolarisation. This form of LTP is prevented by NMDA receptor antagonists and by chelating Ca2+ in the postsynaptic neurone. It is manifest primarily as an increase in the frequency of mEPSCs.
突触传递的长时程增强（LTP）正在接受深入研究。人们认为，其诱导和表达所涉及的机制在对学习、记忆及其他生理功能至关重要的突触过程中起着关键作用。在离体培养神经元中诱导LTP的可靠方法将有助于对LTP分子基础的研究，但一直难以实现。在此，我们报告一种利用短暂去极化在出生后离体海马神经元中诱导LTP的机制。这种形式的LTP可被NMDA受体拮抗剂以及通过螯合突触后神经元中的Ca2+所阻断。它主要表现为微小兴奋性突触后电流（mEPSCs）频率的增加。
