Slowed vesicle priming and enhanced synaptic depression at
syntaxin-1B deficient calyceal synapses
Jianli Guo*, Xuefeng Wang, Hao Tian, Jianyuan Sun#
*Presentation author
#contact author: jysun@ibp.ac.cn ; ++86-10-6488-8537
Institute of Biophysics, Chinese Academy of Sciences
State Key Laboratory of Brain and Cognitive Science
Beijing 100101, China
Key words: Syntaxin 1B; exocytosis; priming; synapse; short term plasticity
Abstract
Syntaxin 1(STX1), including STX1A and STX1B, is a SNARE protein located at
presynaptic membrane and considered to be critical for synaptic vesicle priming and
fusion. However, the previous studies have shown that homozygous STX1A KO mice
exhibited no significant phenotype both in synaptic vesicle release and animal survival.
To determine whether /how STX1B functions in vesicle priming and release kinetics , a
STX1B hypomorph mouse line(XT1B) was analyzed. Whole-cell patch clamp recordings
from these STX1B mutant Calyx of Held synapses showed fewer spontaneous
EPSC(mEPSC) and widened action potential-evoked EPSC(eEPSC). Under train stimulations,
STX1B mutation caused reduction of the eEPSC amplitude at steady state and the
enhancement of synaptic depression. Furthermore, STX1B deficiency largely slowed the
recovery of RRP after depletion, suggesting the impairment of vesicle priming . In
summary, this study shows that syntaxin 1B protein, as a critical determinant of vesicle
release efficiency, modulates releasable vesicle priming and vesicle exocytosis.