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A delayed response enhancement during hippocampal presynaptic plasticity in mice.

机译:小鼠海马突触前可塑性期间的延迟反应增强。

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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.
机译:由于增加的释放概率和/或增加的易于释放的突触小泡的供应,化学突触的高频传入刺激通常引起突触功效的短期增加。继之以可能是由于囊泡耗竭引起的突触抑制。我们在此描述了另一种新颖的类型的延迟和短暂反应增强阶段,该阶段发生在成年小鼠CA1海马区的切片中,在兴奋性谷氨酸能突触的5-20 Hz频率的长时间刺激过程中。第二个增强阶段是在生理温度下最清楚地定义的,而在24摄氏度时基本上不存在,这取决于F-肌动蛋白丝和突触蛋白I和/或II的存在,并且不能归因于突触前动作电位的变化。 ,抑制性神经传递或谷氨酸受体脱敏。时程研究表明,在刺激序列启动后的3-4 s内,延迟的响应阶段中断了突触的衰减,当以5-10 Hz的频率进行检查时,该阶段持续了约75个刺激。新的反应增强可能源自突触小泡的有限池,可以在兴奋性突触活动的延长期间维持突触功效。

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