Sarrazin C
Neurol Res. 1983;5(2):45-78. doi: 10.1080/01616412.1983.11739641.
A mathematical model of facilitation and depression of postsynaptic potential amplitude (PSP) during and following repetitive stimulation is proposed. The model uses first-degree linear equations to simulate the interactions of different presynaptic physiological mechanisms that may influence and control the amount of transmitters liberated outside the nerve terminal. These mechanisms are: (1) vesicle movement toward the presynaptic membrane, (2) transmitter release, (3) vesicle recycling within the synapse, and (4) transmitter synthesis. When submitted to the same frequencies and durations of stimulation as used in a variety of electrophysiological studies of synaptic facilitation and depression, the model successfully reproduces all the variations of PSP amplitude obtained in these studies. The analysis of the internal functioning of the model during the process of simulation also allows a better understanding of the dynamics of diverse phenomena characterizing facilitation and depression during and following the administration of a tetanus. The main conclusion of this study is that both facilitation and depression may be explained in terms of the dynamics of a single synaptic system.
提出了一个关于重复刺激期间及之后突触后电位幅度(PSP)增强和抑制的数学模型。该模型使用一阶线性方程来模拟不同突触前生理机制之间的相互作用,这些机制可能影响和控制神经末梢外释放的递质数量。这些机制包括:(1)囊泡向突触前膜移动;(2)递质释放;(3)突触内囊泡循环;(4)递质合成。当该模型接受与各种突触增强和抑制的电生理研究中使用的相同频率和持续时间的刺激时,它成功地再现了这些研究中获得的PSP幅度的所有变化。对模拟过程中模型内部功能的分析也有助于更好地理解破伤风注射期间及之后表征增强和抑制的各种现象的动态变化。本研究的主要结论是,增强和抑制都可以用单个突触系统的动态变化来解释。