An antagonism between Spinophilin and Syd-1 operates upstream of memory-promoting presynaptic long-term plasticity DOI Creative Commons
Niraja Ramesh, Marc Escher, Oriane Turrel

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2023, Номер unknown

Опубликована: Янв. 27, 2023

Abstract We still face fundamental gaps in understanding how molecular plastic changes of synapses intersect with circuit operation to define behavioral states. Here we show that an antagonism between two conserved regulatory proteins, Spinophilin (Spn) and Syd-1, controls presynaptic long-term plasticity the maintenance olfactory memories Drosophila . While Spn mutants could not trigger nanoscopic active zone remodeling under homeostatic challenge failed stably potentiate neurotransmitter release, concomitant reduction Syd-1 rescued all these deficits. The Spn/Syd-1 converged on close F-actin, genetic or acute pharmacological depolymerization F-actin deficits by allowing access synaptic vesicle release sites. Within intrinsic mushroom body neurons, specifically controlled memory stabilization but initial learning. Thus, this evolutionarily protein complex behaviorally relevant plasticity, also observed mammalian brain enigmatic concerning its mechanisms relevance.

Язык: Английский

An antagonism between Spinophilin and Syd-1 operates upstream of memory-promoting presynaptic long-term plasticity DOI Creative Commons
Niraja Ramesh, Marc Escher, Oriane Turrel

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2023, Номер unknown

Опубликована: Янв. 27, 2023

Abstract We still face fundamental gaps in understanding how molecular plastic changes of synapses intersect with circuit operation to define behavioral states. Here we show that an antagonism between two conserved regulatory proteins, Spinophilin (Spn) and Syd-1, controls presynaptic long-term plasticity the maintenance olfactory memories Drosophila . While Spn mutants could not trigger nanoscopic active zone remodeling under homeostatic challenge failed stably potentiate neurotransmitter release, concomitant reduction Syd-1 rescued all these deficits. The Spn/Syd-1 converged on close F-actin, genetic or acute pharmacological depolymerization F-actin deficits by allowing access synaptic vesicle release sites. Within intrinsic mushroom body neurons, specifically controlled memory stabilization but initial learning. Thus, this evolutionarily protein complex behaviorally relevant plasticity, also observed mammalian brain enigmatic concerning its mechanisms relevance.

Язык: Английский

Процитировано

0