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- W2725118958 abstract "There have been few investigations of the short-term plasticity of synaptic transmission at amphibian sympathetic ganglionic cells where the frequency of miniature excitatory postsynaptic potentials is too low to measure an accurate quantum size. This has made it difficult to investigate the mechanism of synaptic transmission at the ganglionic cells by quantal analysis. A theoretical equation, therefore, is proposed. This equation is based on the premise that transmitter release is due to the product of two factors: intracellular calcium ([Ca2+]i) and acetylcholine (ACh), which is a readily releasable transmitter. The equation accounts for the mechanism of synaptic facilitation and depression of transmitter release at the ganglionic cells in the paired-pulse experiments. The purpose of the present experiment is to investigate whether the equation accounts for the mechanism of short-term plasticity of synaptic transmission produced by a train of pulses at the ganglionic cells. Trains of excitatory postsynaptic current (EPSC) were recorded, and the ratios of the nth EPSC induced by the nth pulse to the initial EPSC were analyzed by the equation. The results indicated that the mechanism of short-term facilitation and depression was interpreted by the equation, which met the following two requirements: [Ca2+]i consisting of two components of residual Ca2+ and the mobilization rate of ACh which accelerated as stimulus frequencies increased. The findings were consistent with those clarified by the quantal analysis. It is suggested that the theoretical equation is also useful for the investigation of the effect of chemical substances on synaptic transmission." @default.
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- W2725118958 date "2017-10-01" @default.
- W2725118958 modified "2023-10-17" @default.
- W2725118958 title "Short-term facilitation and depression of transmitter release at amphibian sympathetic ganglionic cells – Mathematical/computational modeling" @default.
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- W2725118958 doi "https://doi.org/10.1016/j.brainres.2017.06.028" @default.
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