钙/钙调蛋白依赖性蛋白激酶II的α亚基增强大鼠神经元体外γ-氨基丁酸及抑制性突触反应。

Alpha-subunit of calcium/calmodulin-dependent protein kinase II enhances gamma-aminobutyric acid and inhibitory synaptic responses of rat neurons in vitro.

Wang R A, Cheng G, Kolaj M, Randić M

Department of Veterinary Physiology and Pharmacology, Iowa State University, Ames 50011, USA.

J Neurophysiol. 1995 May;73(5):2099-106. doi: 10.1152/jn.1995.73.5.2099.

Abstract

Here we report that in acutely isolated rat spinal dorsal horn neurons, the gamma-aminobutyric acid-A (GABAA) receptor can be regulated by calcium/calmodulin-dependent protein kinase II (CaM-KII). Intracellularly applied, the alpha-subunit of CaM-KII enhanced GABAA-receptor-activated current recorded with the use of the whole cell patch-clamp technique. This effect was associated with reduced desensitization of GABA responses. 2. GABA-induced currents are also potentiated by calyculin A, an inhibitor of protein phosphatases 1 and 2A. 3. Conventional intracellular recordings were made from hippocampal CA1 neurons in slices to determine the effect of intracellular application of CaM-KII on inhibitory synaptic potentials evoked by electrical stimulation of the stratum oriens/alveus. The inhibitory synaptic potential was enhanced by CaM-KII; this mechanism may contribute to long-term enhancement of inhibitory synaptic transmission and may also play a role in other forms of plasticity in the mammalian brain.

摘要

在此我们报告，在急性分离的大鼠脊髓背角神经元中，γ-氨基丁酸-A（GABAA）受体可受钙/钙调蛋白依赖性蛋白激酶II（CaM-KII）调控。在细胞内应用时，CaM-KII的α亚基增强了采用全细胞膜片钳技术记录的GABAA受体激活电流。该效应与GABA反应脱敏作用的降低相关。2. GABA诱导的电流也会被蛋白磷酸酶1和2A的抑制剂冈田酸增强。3. 从脑片上的海马CA1神经元进行传统的细胞内记录，以确定细胞内应用CaM-KII对刺激海马原层/海马槽诱发的抑制性突触电位的影响。CaM-KII增强了抑制性突触电位；该机制可能有助于抑制性突触传递的长期增强，并且可能在哺乳动物脑的其他形式可塑性中发挥作用。