abstract
- Presynaptic Ca(2+) influx pathways, cytoplasmic Ca(2+) buffering proteins and Ca(2+) extrusion processes undergo considerable change during the first postnatal month in rodent neurons. These changes may be critical in establishing short-term plasticity at maturing presynaptic terminals where neurotransmitter release is directly dependent on the dynamics of cytoplasmic residual Ca(2+) ([Ca(2+)](res)). In particular, the robust paired-pulse facilitation characteristic of adult neurons is almost entirely lacking in newborns. To examine developmental changes in processes controlling [Ca(2+)](res), we measured the timecourse of [Ca(2+)](res) decay in presynaptic terminals of Schaffer collateral to CA1 synapses in acute hippocampal slices following single and paired orthodromic stimuli in the stratum radiatum. Developmental changes were observed in both the rise time and slow exponential decay components of the response to single stimuli such that this decay was larger and faster in the adult. Furthermore, we observed a greater caffeine-sensitive basal Ca(2+) store, which was differentially affected when active uptake into the endoplasmic reticulum was blocked, in the presynaptic fields of the Schaffer collateral to CA1 terminals of P6 and younger mice when compared to adults. These transitions in [Ca(2+)](res) dynamics occurred gradually over the first weeks of postnatal life and correlated with changes in short-term plasticity.