mlck-peptide and calmidazolium

Repetitive nerve firings cause short-term depression (STD) of release at many synapses. Its underlying mechanism is largely attributed to depletion of a readily releasable vesicle pool (RRP) and a decreased probability of releasing a readily releasable vesicle during an action potential. Which of these two mechanisms is dominant and the mechanism that decreases the release probability remain debated. Here, we report that a decreased release probability is caused by a calcium-induced inhibition of presynaptic calcium channels, particularly P/Q-type channels at the calyx of Held in rat brainstem. This mechanism was the dominant cause of STD in a wide range of stimulation conditions, such as during 2 to 20 action potential-equivalent stimuli (AP-e) at 0.2-30 Hz and after 2 to 20 AP-e at 0.2-100 Hz. Only during > or = 100 Hz AP-e was depletion the dominant mechanism.

Topics: Action Potentials; Animals; Animals, Newborn; Barium; Brain Stem; Calcium; Calcium Channels; Chelating Agents; CREB-Binding Protein; Dose-Response Relationship, Radiation; Egtazic Acid; Electric Capacitance; Electric Stimulation; Enzyme Inhibitors; Imidazoles; In Vitro Techniques; Models, Biological; Neural Inhibition; Nuclear Proteins; Patch-Clamp Techniques; Peptides; Presynaptic Terminals; Rats; Rats, Wistar; Synapses; Time Factors; Trans-Activators