Development of presynaptic calcium dynamics and short-term plasticity in the SC-Ca1 synapse
Year: 2010
Type: article
Abstract: Following a presynaptic action potential, there is a rapid rise of [Ca2+]i in the immediate vicinity of Ca2+ channels that triggers membrane fusion and release of transmitter from vesicles within this microdomain. This presynaptic Ca2+ signal ([Ca2+]pre) then disperses to produce a residual Ca2+ ([Ca2+]res) that decays over the course of tens to hundreds of milliseconds. The [Ca2+]res has important implications in synaptic plasticity and is the basis for working memory storage. Ultimately [Ca2+]res is removed from the cytoplasm either into intracellular organelles or across the plasma membrane into the extracellular environment. Calcium influx pathways, cytoplasmic Ca2+ buffering proteins, and Ca2+ extrusion processes in rodent neurons undergo considerable change during the first postnatal month. These changes have important functional significance in short-term plasticity — in particular paired-pulse facilitation (PPF) — at presynaptic terminals where neurotransmitter release is directly dependent on the dynamics of free cytoplasmic Ca2+. To examine developmental changes in [Ca2+]res dynamics in the Schaffer collateral synapses onto CA1 pyramidal neurons in in vitro hippocampal slices, we measured the timecourse of decay of [Ca2+]res in presynaptic terminals following single and paired orthodromic stimuli in the stratum radiatum. The contribution of the slow component compared to the total decay of [Ca2+]res was reduced from >80% in newborn mice to ~50% in the more mature animals (>P24) and [Ca2+]res had a distinct slow rising component in newborn mice (
Author: Chessa Scullin
Language: English
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
Funder: National Institutes of Health
OpenAlex ID: W579287748