Abstract
Synaptic vesicle (SV) release probability (Pr) is a key presynaptic determinant of synaptic strength established by cell-intrinsic properties and further refined by plasticity. To characterize mechanisms that generate Pr heterogeneity between distinct neuronal populations, we examined glutamatergic tonic (Ib) and phasic (Is) motoneurons in Drosophila with stereotyped differences in Pr and synaptic plasticity. We found the decoy soluble N-ethylmaleimide sensitive factor attachment protein receptor (SNARE) Tomosyn is differentially expressed between these motoneuron subclasses and contributes to intrinsic differences in their synaptic output. Tomosyn expression enables tonic release in Ib motoneurons by reducing SNARE complex formation and suppressing Pr to generate decreased levels of SV fusion and enhanced resistance to synaptic fatigue. In contrast, phasic release dominates when Tomosyn expression is low, enabling high intrinsic Pr at Is terminals at the expense of sustained release and robust presynaptic potentiation. In addition, loss of Tomosyn disrupts the ability of tonic synapses to undergo presynaptic homeostatic potentiation.
Highlights
Ca2+-dependent fusion of synaptic vesicles (SVs) is the primary mechanism for neurotransmission and is mediated by the soluble N-ethylmaleimide sensitive factor attachment protein receptor (SNARE) family (Jahn and Scheller, 2006; Söllner et al, 1993; Sudhof, 2004; Weber et al, 1998)
Stereotyped differences in probability of SV fusion (Pr) exist across neurons, with many neuronal populations broadly classified as tonic or phasic depending on their spiking patterns, Pr and short-term plasticity characteristics (Atwood and Karunanithi, 2002; Dittman et al, 2000; Lnenicka and Keshishian, 2000)
The Drosophila Tomosyn homolog is highly conserved with other Tomosyn proteins, displaying high sequence conservation in critical domains including the C-terminal SNARE motif
Summary
Ca2+-dependent fusion of synaptic vesicles (SVs) is the primary mechanism for neurotransmission and is mediated by the soluble N-ethylmaleimide sensitive factor attachment protein receptor (SNARE) family (Jahn and Scheller, 2006; Söllner et al, 1993; Sudhof, 2004; Weber et al, 1998). The postsynaptic cell controls sensitivity to neurotransmitters by governing receptor field composition, while the presynaptic neuron establishes the probability of SV fusion (Pr) (Citri and Malenka, 2008; Körber and Kuner, 2016; Nicoll, 2003; Yang and Calakos, 2013). How cell-intrinsic properties establish differences in presynaptic Pr between neuronal classes, and how release strength is further refined via plasticity, remain incompletely understood
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
