Pereda A E, Bell T D, Chang B H, Czernik A J, Nairn A C, Soderling T R, Faber D S
Allegheny University of the Health Sciences, Philadelphia, PA 19129, USA.
Proc Natl Acad Sci U S A. 1998 Oct 27;95(22):13272-7. doi: 10.1073/pnas.95.22.13272.
While chemical synapses are very plastic and modifiable by defined activity patterns, gap junctions, which mediate electrical transmission, have been classically perceived as passive intercellular channels. Excitatory transmission between auditory afferents and the goldfish Mauthner cell is mediated by coexisting gap junctions and glutamatergic synapses. Although an increased intracellular Ca2+ concentration is expected to reduce gap junctional conductance, both components of the synaptic response were instead enhanced by postsynaptic increases in Ca2+ concentration, produced by patterned synaptic activity or intradendritic Ca2+ injections. The synaptically induced potentiations were blocked by intradendritic injection of KN-93, a Ca2+/calmodulin-dependent kinase (CaM-K) inhibitor, or CaM-KIINtide, a potent and specific peptide inhibitor of CaM-KII, whereas the responses were potentiated by injection of an activated form of CaM-KII. The striking similarities of the mechanisms reported here with those proposed for long-term potentiation of mammalian glutamatergic synapses suggest that gap junctions are also similarly regulated and indicate a primary role for CaM-KII in shaping and regulating interneuronal communication, regardless of its modality.
虽然化学突触具有很强的可塑性，并可通过特定的活动模式进行修饰，但介导电传递的缝隙连接传统上被视为被动的细胞间通道。听觉传入神经与金鱼毛特纳细胞之间的兴奋性传递由共存的缝隙连接和谷氨酸能突触介导。虽然细胞内Ca2+浓度升高预计会降低缝隙连接的电导，但突触反应的两个组成部分反而因模式化突触活动或树突内Ca2+注射产生的突触后Ca2+浓度升高而增强。突触诱导的增强作用被树突内注射Ca2+/钙调蛋白依赖性激酶（CaM-K）抑制剂KN-93或CaM-KII的强效特异性肽抑制剂CaM-KIINtide所阻断，而通过注射活化形式的CaM-KII可增强反应。此处报道的机制与哺乳动物谷氨酸能突触长时程增强所提出的机制惊人相似，这表明缝隙连接也受到类似调节，并表明CaM-KII在塑造和调节神经元间通讯中起主要作用，而不论其方式如何。
