Presynaptic Plasticity Is Associated with Actin Polymerization

Modulation of presynaptic short-term plasticity induced by actin polymerization was studied in rat hippocampal slices using the paired-pulse paradigm. Schaffer collaterals were stimulated with paired pulses with a 70-ms interstimulus interval every 30 s before and during perfusion with jasplakinolide, an activator of actin polymerization. Jasplakinolide application resulted in the increase in the amplitudes of CA3-CA1 responses (potentiation) accompanied by a decrease in the paired-pulse facilitation, suggesting induction of presynaptic modifications. Jasplakinolide-induced potentiation depended on the initial paired-pulse rate. These data indicate that the jasplakinolide-mediated changes in actin polymerization increased the probability of neurotransmitter release. Less typical for CA3-CA1 synapses responses, such as a very low paired-pulse ratio (close to 1 or even lower) or even paired-pulse depression, were affected differently. Thus, jasplakinolide caused potentiation of the second, but not the first response to the paired stimulus, which increased the paired-pulse ratio from 0.8 to 1.0 on average, suggesting a negative impact of jasplakinolide on the mechanisms promoting paired-pulse depression. In general, actin polymerization facilitated potentiation, although the patterns of potentiation differed depending on the initial synapse characteristics. We conclude that in addition to the increase in the neurotransmitter release probability, jasplakinolide induced other actin polymerization-dependent mechanisms, including those involved in the paired-pulse depression.