Synaptic plasticity at crayfish neuromuscular junctions: facilitation and augmentation.
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abstract
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 only slight increases in the peak voltage and duration of APs for the 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 presynaptic terminal exhibits 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., accumulation of ions, changes in ionic conductances, etc.) may be partly responsible for augmentation of EPSP amplitudes.
