Patneau D K, Mayer M L
Laboratory of Developmental Neurobiology, National Institutes of Health, Bethesda, Maryland 20892.
Neuron. 1991 May;6(5):785-98. doi: 10.1016/0896-6273(91)90175-y.
AMPA but not kainate produces a rapidly desensitizing response in mouse hippocampal neurons. The characteristic action of these agonists appears to arise from activation of a single receptor with active and desensitized states, for which AMPA and kainate have different relative affinity. The equilibrium potency of a series of five agonists that produce rapidly desensitizing responses at non-NMDA receptors (EC50 1 microM to 4 mM) was similar to their equilibrium potency for block of kainate responses. Increasing the concentration of kainate overcame such block, but in the presence of AMPA the rate of activation of responses to kainate was slowed. Conversely, in the presence of kainate the amplitude of rapidly desensitizing responses evoked by AMPA was reduced, and the rate of onset of desensitization was slowed.
α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)而非海人藻酸(kainate)能在小鼠海马神经元中产生快速脱敏反应。这些激动剂的特征性作用似乎源于单一受体的激活,该受体具有活性状态和脱敏状态,AMPA和海人藻酸对其具有不同的相对亲和力。在非N-甲基-D-天冬氨酸(NMDA)受体上产生快速脱敏反应的一系列五种激动剂(半数有效浓度[EC50]为1微摩尔至4毫摩尔)的平衡效价与其阻断海人藻酸反应的平衡效价相似。增加海人藻酸的浓度可克服这种阻断,但在存在AMPA的情况下,对海人藻酸反应的激活速率会减慢。相反,在存在海人藻酸的情况下,AMPA诱发的快速脱敏反应的幅度会降低,脱敏起始速率也会减慢。