Paired‐pulse facilitation and depression at unitary synapses in rat hippocampus: quantal fluctuation affects subsequent release.

Abstract

3. When two action potentials were elicited in the presynaptic cell, the amplitude of the second EPSC was inversely related to the amplitude of the first. Paired-pulse facilitation (PPF) was observed when the first EPSC was small, i.e. the second EPSC was larger than the first, whereas paired-pulse depression (PPD) was observed when the first EPSC was large. 4. The number of trials displaying PPD was greater when release probability was increased, and smaller when release probability was decreased. 5. PPD was not postsynaptically mediated because it was unaffected by decreasing ionic flux with 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) or receptor desensitization with aniracetam.6. PPF was maximal at an interstimulus interval of 70 ms and recovered within 500 ms. Recovery from PPD occurred within 5 s. 7. We propose that multiple release sites are formed by the axon of a CA3 pyramidal cell and a single postsynaptic CAl or CA3 cell. PPF is observed if the first action potential fails to release transmitter at most release sites. PPD is observed if the first action potential successfully triggers release at most release sites. 8. Our observations of PPF are consistent with the residual calcium hypothesis. We conclude that PPD results from a decrease in quantal content, perhaps due to short-term depletion of readily releasable vesicles.

Short-Term Presynaptic Plasticity

“…Thus, the depletion model predicts a negative correlation between EPSC2 and EPSC1 for two closely spaced stimuli. Consistent with this prediction, a negative correlation between the amplitudes of two closely spaced EPSCs has been observed at the neuromuscular junction (Elmqvist and Quastel 1965), hair cell synapses (Furukawa et al 1978), the calyx of Held (Scheuss et al 2002), thalamocortical synapses (Ran et al 2009), cortical connections (Thomson et al 1993), and hippocampal synapses (Debanne et al 1996). However, at some synapses the extent of depression does not appear to depend on the magnitude of release evoked by the first stimulus (Thomson and Bannister 1999; Kraushaar and Jonas 2000;Chen et al 2004) or the size of the RRP (Sullivan 2007), and an inverse correlation has not been seen at synapses onto Mauthner cells (Waldeck et al 2000) and at hippocampal synapses (Chen et al 2004).…”

Ethanol increases GABAergic transmission at both pre- and postsynaptic sites in rat central amygdala neurons

“…To determine whether ethanol changes the probability of GABA release at CeA synapses, we carried out three types of experiments. In the first set of experiments we examined PPF (at an interpulse interval of 50 msec), a phenomenon whereby a secondary synaptic response is increased by a preceding primary stimulation of equal intensity (23)(24)(25). Changes in PPF are inversely related to transmitter release such that a reduction of PPF is associated with an increased probability of transmitter release (26,27).…”

Long-term potentiation involves increases in the probability of neurotransmitter release

“…Evidence for this comes from examining quantal parameters (5,(31)(32)(33)(34)(35), presynaptic calcium transients during PPF (36), and the effect of altering membrane potential (37), and from finding that maneuvers that alter p are associated with changes in PPF (11,12,38). However, there is also evidence for a postsynaptic component to its expression (39).…”