Activity-dependent modulation of the presynaptic potassium current in the frog neuromuscular junction.
1. Changes in the electrical properties of frog motor nerve endings caused by the invasion of an action potential were studied by the perineural recording technique. Two equal supramaximal stimuli separated by a variable time interval were applied to the nerve trunk. The latency and amplitude of the deflections associated with the nodal Na+ current and presynaptic K+ current elicited by the second pulse were compared with control currents. 2. The deflection associated with the presynaptic K+ current elicited in response to the second stimulus was absent at the shortest interstimulus interval and showed a progressive increase in its amplitude as the interstimulus interval was lengthened, reaching values greater than control in most terminals. During the same period the nodal Na+ current did not change. 3. The experimental results were compared with a computer model of the distal axonal segment and its terminal. Response of the model to twin-pulse stimulation was in marked disagreement with the experimental results unless an inactivating K+ channel, with properties derived ad hoc, was incorporated into the simulation. 4. These results suggest that in the first 6-7 ms after a nerve impulse has invaded a frog motor nerve ending, maximal K+ conductance remains below the value at rest due to the fast inactivation of a K+ conductance. Following this, there is a period in which K+ conductance is greater than control values although the basis for this is unknown.
Departament de Biologia Cellular i Anatomia Patològica, Facultat de Medicina, Hospital de Bellvitge, Universitat de Barcelona, Spain.
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F
Miralles
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C
Solsona
D015761:4-Aminopyridine / Q000031:analogs & derivatives / Q000494:pharmacology; D000200:Action Potentials; D000077770:Amifampridine; D000818:Animals; D001369:Axons / Q000378:metabolism; D003198:Computer Simulation; D004558:Electric Stimulation; D066298:In Vitro Techniques; D017136:Ion Transport; D007700:Kinetics; D008959:Models, Neurological; D009431:Neural Conduction; D009469:Neuromuscular Junction / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000378:metabolism; D017729:Presynaptic Terminals / Q000378:metabolism*; D011898:Ranidae; D012964:Sodium / Q000378:metabolism
D026902:Potassium Channel Blockers; D015221:Potassium Channels; D012964:Sodium; D015761:4-Aminopyridine; D000077770:Amifampridine; D011188:Potassium