Abstract
Much of what we know about the mechanisms underlying Homosynaptic Depression (HSD) and heterosynaptic facilitation is based on intracellular recordings of integrated postsynaptic potentials (PSPs). This methodological approach views the presynaptic apparatus as a single compartment rather than taking a more realistic representation reflecting the fact that it is made up of tens to hundreds of individual and independent Presynaptic Release Boutons (PRBs). Using cultured Aplysia sensorimotor synapses, we reexamined HSD and its dishabituation by imaging the release properties of individual PRBs. We find that the PRB population is heterogeneous and can be clustered into three groups: ~25% of the PRBs consistently release neurotransmitter throughout the entire habituation paradigm (35 stimuli, 0.05 Hz) and have a relatively high quantal content, 36% of the PRBs display intermittent failures only after the tenth stimulation, and 39% are low quantal-content PRBs that exhibit intermittent release failures from the onset of the habituation paradigm. 5HT-induced synaptic dishabituation by a single 5HT application was generated by the enhanced recovery of the quantal content of the habituated PRBs and did not involve the recruitment of new release boutons. The characterization of the PRB population as heterogeneous in terms of its temporal pattern of release-probability and quantal content provides new insights into the mechanisms underlying HSD and its dishabituation.
Highlights
Homosynaptic depression (HSD or synaptic habituation) and its dishabituation by neuromodulators are conserved forms of learning and memory mechanisms at the synaptic level (Kandel, 2001; Fioravante and Regehr, 2011; Regehr, 2012)
To facilitate the imaging of the Excitatory Post-Synaptic Calcium concentration Transient (EPSCaT), the experiments were performed in artificial sea water (ASW) in which the calcium concentration was 55 mM, instead of 11 mM and www.frontiersin.org the magnesium concentration was reduced to 11 mM
Consistent with earlier studies that reported that this concentration of divalent ions does not change synaptic strength (Jiang and Abrams, 1998; Royer et al, 2000), we found that the SN-L7 synapses underwent Homosynaptic Depression (HSD) in high Ca-ASW with the same kinetics as in normal ASW
Summary
Homosynaptic depression (HSD or synaptic habituation) and its dishabituation by neuromodulators are conserved forms of learning and memory mechanisms at the synaptic level (Kandel, 2001; Fioravante and Regehr, 2011; Regehr, 2012). Because of the electro-anatomical properties of most neurons, intracellularly recorded PSPs are inevitably the integral of evoked neurotransmitter release from tens to hundreds of presynaptic boutons. Conventional intracellular recordings do not permit analysis of the release behavior of individual presynaptic boutons during HSD and synaptic dishabituation. The number of synaptic boutons formed between the SN and L7 is in the range of 30–40 (Kim et al, 2003; Malkinson and Spira, 2010a) and are spaced at 5–15 μm intervals (Malkinson and Spira, 2010a,b). PSPs recorded by an intracellular microelectrode represent an integral in time and space of an unknown number of individual active presynaptic boutons
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