Jensen Vidar, Walaas S Ivar, Hilfiker Sabine, Ruiz Arnaud, Hvalby Øivind
Molecular Neurobiology Research Group (MONERG), PO Box 1104, Faculty of Medicine, University of Oslo, N-0317 Blindern, Oslo, Norway.
J Physiol. 2007 Aug 15;583(Pt 1):129-43. doi: 10.1113/jphysiol.2007.131300. Epub 2007 Jun 14.
High frequency afferent stimulation of chemical synapses often induces short-term increases in synaptic efficacy, due to increased release probability and/or increased supply of readily releasable synaptic vesicles. This may be followed by synaptic depression, often caused by vesicle depletion. We here describe an additional, novel type of delayed and transient response enhancement phase which occurred during prolonged stimulation at 5-20 Hz frequency of excitatory glutamatergic synapses in slices from the adult mouse CA1 hippocampal region. This second enhancement phase, which was most clearly defined at physiological temperatures and essentially absent at 24 degrees C, was dependent on the presence of F-actin filaments and synapsins I and/or II, and could not be ascribed to changes in presynaptic action potentials, inhibitory neurotransmission or glutamate receptor desensitization. Time course studies showed that the delayed response phase interrupted the synaptic decay 3-4 s after stimulus train initiation and continued, when examined at 5-10 Hz frequencies, for approximately 75 stimuli before decay. The novel response enhancement, probably deriving from a restricted pool of synaptic vesicles, may allow maintenance of synaptic efficacy during prolonged periods of excitatory synaptic activity.
化学突触的高频传入刺激通常会导致突触效能短期增加,这是由于释放概率增加和/或易释放突触囊泡的供应增加。随后可能会出现突触抑制,这通常是由囊泡耗竭引起的。我们在此描述了一种额外的、新型的延迟和短暂反应增强阶段,该阶段发生在成年小鼠CA1海马区切片中兴奋性谷氨酸能突触以5-20Hz频率进行长时间刺激期间。这个第二个增强阶段在生理温度下最为明显,在24摄氏度时基本不存在,它依赖于F-肌动蛋白丝以及突触结合蛋白I和/或II的存在,并且不能归因于突触前动作电位、抑制性神经传递或谷氨酸受体脱敏的变化。时间进程研究表明,延迟反应阶段在刺激序列开始后3-4秒中断突触衰减,当以5-10Hz频率进行检测时,在衰减前持续约75次刺激。这种新的反应增强可能源于有限的突触囊泡池,它可能在长时间的兴奋性突触活动期间维持突触效能。