RT Journal Article SR Electronic T1 The Lack of Synapsin Alters Presynaptic Plasticity at Hippocampal Mossy Fibers in Male Mice JF eneuro JO eNeuro FD Society for Neuroscience SP ENEURO.0330-23.2024 DO 10.1523/ENEURO.0330-23.2024 VO 11 IS 7 A1 Bruentgens, Felicitas A1 Moreno Velasquez, Laura A1 Stumpf, Alexander A1 Parthier, Daniel A1 Breustedt, Jörg A1 Benfenati, Fabio A1 Milovanovic, Dragomir A1 Schmitz, Dietmar A1 Orlando, Marta YR 2024 UL http://www.eneuro.org/content/11/7/ENEURO.0330-23.2024.abstract AB Synapsins are highly abundant presynaptic proteins that play a crucial role in neurotransmission and plasticity via the clustering of synaptic vesicles. The synapsin III isoform is usually downregulated after development, but in hippocampal mossy fiber boutons, it persists in adulthood. Mossy fiber boutons express presynaptic forms of short- and long-term plasticity, which are thought to underlie different forms of learning. Previous research on synapsins at this synapse focused on synapsin isoforms I and II. Thus, a complete picture regarding the role of synapsins in mossy fiber plasticity is still missing. Here, we investigated presynaptic plasticity at hippocampal mossy fiber boutons by combining electrophysiological field recordings and transmission electron microscopy in a mouse model lacking all synapsin isoforms. We found decreased short-term plasticity, i.e., decreased facilitation and post-tetanic potentiation, but increased long-term potentiation in male synapsin triple knock-out (KO) mice. At the ultrastructural level, we observed more dispersed vesicles and a higher density of active zones in mossy fiber boutons from KO animals. Our results indicate that all synapsin isoforms are required for fine regulation of short- and long-term presynaptic plasticity at the mossy fiber synapse.