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Presynaptic and postsynaptic mechanisms underlie paired pulse depression at single GABAergic boutons in rat collicular cultures

2002; Wiley; Volume: 543; Issue: 1 Linguagem: Inglês

10.1113/jphysiol.2002.021576

1469-7793

Sergei Kirischuk, John D. Clements, Rosemarie Grantyn,

Neuroscience and Neural Engineering

Paired pulse depression (PPD) is a common form of short‐term synaptic plasticity. The aim of this study was to characterise PPD at the level of a single inhibitory bouton. Low‐density collicular cultures were loaded with the Ca 2+ indicator Oregon Green‐1, active boutons were stained with RH414, and action potentials were blocked with TTX. Evoked IPSCs (eIPSCs) and presynaptic Ca 2+ transients were recorded in response to direct presynaptic depolarisation of an individual bouton. The single bouton eIPSCs had a low failure rate (< 0.1), large average quantal content (3‐6) and slow decay (τ 1 = 15 ms, τ 2 = 81 ms). The PPD of eIPSCs had two distinct components: PPD fast and PPD slow (τ= 86 ms and 2 s). PPD slow showed no dependence on extracellular Ca 2+ concentration, or on the first eIPSC's failure rate or amplitude. Most probably, it reflects a release‐independent inhibition of exocytosis. PPD fast was only observed in normal or elevated Ca 2+ . It decreased with the failure rate and increased with the amplitude of the first eIPSC. It coincided with paired pulse depression of the presynaptic Ca 2+ transients (τ= 120 ms). The decay of the latter was accelerated by EGTA, which also reduced PPD fast . Therefore, a suppressive effect of residual presynaptic Ca 2+ on subsequent Ca 2+ influx is considered the most likely cause of PPD fast . PPD fast may also have a postsynaptic component, because exposure to a low‐affinity GABA A receptor antagonist (TPMPA; 300 μM) counteracted PPD fast , and asynchronous IPSC amplitudes were depressed for a short interval following an eIPSC. Thus, at these synapses, PPD is produced by at least two release‐independent presynaptic mechanisms and one release‐dependent postsynaptic mechanism.