Synaptic plasticity at crayfish neuromuscular junctions: facilitation and augmentation.
Synaptic plasticity at crayfish neuromuscular junctions: facilitation and augmentation.
复制标题
小龙虾神经肌肉接头的突触可塑性:促进和增强。
DOI:
10.1002/syn.890070308
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发表时间:
1991
期刊:
影响因子:
--
通讯作者:
Baxter,DA
中科院分区:
文献类型:
--
作者:
Bittner,GD;Baxter,DA
Simultaneous intracellular recordings from presynaptic nerve terminals and postsynaptic muscle fibers were used to investigate the extent to which changes in presynaptic voltage may contribute to short‐term facilitation and augmentation of transmitter release at neuromuscular junctions of the crayfish (Procambarus simulans) opener muscle. Presynaptic nerve terminals have an average resting membrane potential of about–80 mV, single action potentials have an average foot‐to‐peak amplitude of about 98 mV, and single action potentials are followed by a depolarizing after potential (DAP) of about 10 mV. During stimulus trains of 9–16 impulses at 100 Hz, amplitudes of excitatory postsynaptic potentials (EPSPs) continuously facilitate up to 100‐fold. This dramatic facilitation is associated with oly slight increases in the peak voltage and duration of APs for first 2–4 pulses in such a stimulus train. Foot‐to‐peak total amplitude of APs usually decreases after the first pulse in a stimulus train. The data strongly suggest that short‐term facilitation is not due to changes in the amplitude or duration of APs invading the presynaptic terminal. Upon cessation of a longer stimulus train, the presnaptic terminal exh‐ibits a hyperpolarizing after potential (HAP) up to 16 mV in amplitude depending upon the frequency (10–100 Hz) and duration (1–10 sec) of the tetanic stimulation. This post‐tetanic HAP decays with a time constant of 10–20 sec, which is approximately equal to the third time constant of decay in EPSP amplitude (augmentation) following tetanic stimulation. Hence, presynaptic voltage changes and/or processes associated with these voltage changes (e.g., acumulation of ions, changes in ionic conductances, etc.) may be responsible for augmentation of EPSP amplitudes.