A Novel Form of Presynaptic Plasticity Based on the Fast Reactivation of Release Sites Switched Off during Low-Frequency Depression

• DOI: 10.1523/jneurosci.3644-09.2010
• Publication Date: 2010-12-08T17:50:17Z
• Authors: Frédéric Doussau; Yann Humeau; Fabio Benfenati; Bernard Poulain
• Keywords: Synapsin; Aplysia; Neural facilitation

Repetitive firing of neurons at a low frequency often leads to decrease in synaptic strength. The mechanism this low-frequency depression (LFD) is poorly understood. Here, LFD was studied Aplysia cholinergic synapses. absence significant change the paired-pulse ratio during LFD, together with facts that neither time course nor extent were affected by initial release probability, suggests not related depletion ready-to-fuse vesicles (SVs) or but results from silencing subpopulation sites. A subset SVs sites, which acquired high probability status permits synapses rapidly and temporarily recover strength when stimulation stopped. However, recovery full capacity synapse sustain repetitive stimulations slow involves spontaneous reactivation silent Application tetanic accelerates immediately switching on This high-frequency-dependent phenomenon underlies new form plasticity allows resetting presynaptic efficiency independently recent history synapse. Microinjection mutated synapsin cannot be phosphorylated cAMP-dependent protein kinase (PKA), PKA inhibitor both prevented awakening Changes pattern appear able regulate on–off sites via molecular cascade involving PKA-dependent phosphorylation synapsin.