title: [The mechanisms of short-term forms of synaptic plasticity].
abstract: In experiments on the frog cutaneous pectoris muscle in cases of different external calcium concentrations, using extracellular recording technique, processes of facilitation and depression of transmitter release during the high-frequency stimulation were investigated. On the ground of experiments using intracellular mobile calcium buffers BAPTA-AM and EGTA-AM, it was proposed that at least two (low- and high-affinity) calcium-binding sites underlie the facilitation. Both the facilitation and the depression were accompanied by such transformations of underlied of nerve ending responses as changes of the third phase amplitude. Application of potassium channel blockers allowed us to reveal the significant contribution of changes of duration of the AP repolarisation phase and, accordingly, the changes of magnitude of calcium influx to development of facilitation and depression of transmitter release. It was also revealed that, during the high-frequency rhythmic stimulation, the increase of asynchrony of transmitter release leading to decrease of facilitation and increase of depression occurred. It was concluded that the forms of short-term synaptic plasticity--facilitation and depression, were caused by various presynaptic mechanisms: the increase of concentration of "local" and accumulation of "residual" calcium, the changes of calcium influx, increase of temporal course of secretion, the impairment of equilibrium between the depletion and restoration of mediator supply. Due to some of these processes and specific conditions of synapse functioning, the facilitation of the depression of transmitter release occurred.
authors.forename: A L
authors.initials: AL
authors.lastname: Zefirov
authors.forename: M A
authors.initials: MA
authors.lastname: Mukhamed'iarov
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D002118:Calcium / Q000494:pharmacology / Q000502:physiology*; D004533:Egtazic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D004558:Electric Stimulation; D066298:In Vitro Techniques; D009469:Neuromuscular Junction / Q000187:drug effects / Q000502:physiology*; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D010455:Peptides / Q000494:pharmacology; D010880:Piperidines / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D017729:Presynaptic Terminals / Q000502:physiology; D011895:Rana ridibunda; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*
chemical_list: C481395:4-aminopiperidine; D010455:Peptides; D010880:Piperidines; D026902:Potassium Channel Blockers; C070379:1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; D004533:Egtazic Acid; C064719:iberiotoxin; C046770:EGTA acetoxymethyl ester; D002118:Calcium