Fleck M W, Palmer A M, Barrionuevo G
Department of Behavioral Neuroscience, University of Pittsburgh, PA 15260.
Brain Res. 1992 May 15;580(1-2):100-5. doi: 10.1016/0006-8993(92)90931-x.
We observed that a transient increase in extracellular potassium concentration (50 mM for 40 s) was sufficient to induce long-term potentiation (LTP) of synaptic transmission in area CA1 of the hippocampal slice. Potassium-induced potentiation of the Schaffer collateral/commissural synapses demonstrated several features characteristic of tetanus-induced LTP: (1) population excitatory post-synaptic potential (EPSP) amplitudes were enhanced to a similar magnitude (on average 70% above baseline) which (2) lasted for more than 20 min; (3) induction was blocked by bath application of the specific N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonovalerate (D-APV), and (4) was attenuated by reduction of the concentration of calcium in the extracellular medium. Induction of either potassium-induced LTP or tetanus-induced LTP occluded the subsequent expression of the other. Finally, exposure to high potassium in the absence of electrical stimulation was sufficient to induce LTP. Taken together, these data indicate that brief depolarizing stimuli other than tetanus can induce LTP. Because potassium-induced LTP is not restricted to the subset of afferents examined electrophysiologically, such a method could facilitate analyses of the biochemical events underlying both the induction and expression of LTP.
我们观察到细胞外钾离子浓度的短暂升高（50 mM，持续40秒）足以诱导海马切片CA1区突触传递的长时程增强（LTP）。钾离子诱导的Schaffer侧支/连合突触增强表现出破伤风诱导的LTP的几个特征：（1）群体兴奋性突触后电位（EPSP）幅度增强到相似程度（平均比基线高70%），（2）持续超过20分钟；（3）通过在浴槽中应用特异性N-甲基-D-天冬氨酸（NMDA）受体拮抗剂D-2-氨基-5-磷酸戊酸（D-APV）可阻断诱导，（4）通过降低细胞外培养基中钙的浓度而减弱。钾离子诱导的LTP或破伤风诱导的LTP的诱导会阻断另一种的后续表达。最后，在无电刺激的情况下暴露于高钾足以诱导LTP。综上所述，这些数据表明除破伤风外的短暂去极化刺激可诱导LTP。由于钾离子诱导的LTP不限于通过电生理学检查的传入神经元子集，这种方法可能有助于分析LTP诱导和表达背后的生化事件。
