Carroll R C, Nicoll R A, Malenka R C
Department of Psychiatry, University of California, San Francisco, California 94143, USA.
J Neurophysiol. 1998 Nov;80(5):2797-800. doi: 10.1152/jn.1998.80.5.2797.
Protein kinases play an important role in controlling synaptic strength at excitatory synapses on CA1 pyramidal cells. We examined the effects of activating cAMP-dependent protein kinase or protein kinase C (PKC) on the frequency and amplitude of miniature excitatory postsynaptic currents (mEPSCs) with perforated patch recording techniques. Both forskolin and phorbol-12,13-dibutryate (PDBu) caused a large increase in mEPSC frequency, but only PDBu increased mEPSC amplitude, an effect that was not observed when standard whole cell recording was performed. These results support biochemical observations indicating that PKC, similar to calcium/calmodulin-dependent protein kinase II, has an important role in controlling synaptic strength via modulation of AMPA receptor function, potentially through the direct phosphorylation of the GluR1 subunit.
蛋白激酶在控制CA1锥体细胞兴奋性突触的突触强度方面发挥着重要作用。我们采用穿孔膜片钳记录技术，研究了激活环磷酸腺苷（cAMP）依赖性蛋白激酶或蛋白激酶C（PKC）对微小兴奋性突触后电流（mEPSCs）频率和幅度的影响。福斯高林和佛波醇-12,13-二丁酸酯（PDBu）均使mEPSC频率大幅增加，但只有PDBu增加了mEPSC幅度，而在进行标准全细胞记录时未观察到这种效应。这些结果支持了生化观察结果，表明PKC与钙/钙调蛋白依赖性蛋白激酶II类似，可能通过直接磷酸化GluR1亚基，在通过调节AMPA受体功能来控制突触强度方面发挥重要作用。
