Presynaptic plasticity is associated with actin polymerization

Abstract

Modifications of presynaptic short-term plasticity as a result of actin polymerization were tested in rat hippocampal slices using a paired-pulse paradigm. Paired-pulse stimulation of Schaffer collaterals with 70 ms interpulse interval was continuously presented every 30 s before and during perfusion with jasplakinolide, an activator of actin polymerization. Jasplakinolide application resulted in the potentiation of CA3-CA1 responses accompanied by paired-pulse facilitation decrease, these effects suggesting presynaptic modifications. The jasplakinolide-induced potentiation significantly depended on the initial paired-pulse facilitation values. These data indicate that jasplakinolide-mediated changes in actin polymerization may promote high probability of release. Less typical for CA3-CA1 synapses responses with very low initial paired-pulse facilitation or paired-pulse depression (close to 1 or even lower) demonstrated the potentiation of the second, but not the first amplitude in a pair, paired-pulse ratio significantly increasing from 0.8 to 1.0 in average. This may suggest a negative impact of jasplakinolide on the mechanisms underlying paired-pulse depression. Nonetheless, actin polymerization promotes potentiation, though patterns of this activation may differ depending on initial input characteristics. We conclude that in addition to increased neurotransmitter release probability other mechanisms known to suppress paired pulse facilitation may be also involved in effects of jasplakinolide.