A use-dependent increase in release sites drives facilitation at calretinin-deficient cerebellar parallel-fiber synapses.
A use-dependent increase in release sites drives facilitation at calretinin-deficient cerebellar parallel-fiber synapses.
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DOI:
10.3389/fncel.2015.00027
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发表时间:
2015
影响因子:
5.3
通讯作者:
Schmidt H
中科院分区:
文献类型:
--
作者:
Brachtendorf S;Eilers J;Schmidt H
Endogenous Ca2+-binding proteins affect synaptic transmitter release and short-term plasticity (STP) by buffering presynaptic Ca2+ signals. At parallel-fiber (PF)-to-Purkinje neuron (PN) synapses in the cerebellar cortex loss of calretinin (CR), the major buffer at PF terminals, results in increased presynaptic Ca2+ transients and an almost doubling of the initial vesicular releases probability (pr). Surprisingly, however, it has been reported that loss of CR from PF synapses does not alter paired-pulse facilitation (PPF), while it affects presynaptic Ca2+ signals as well as pr. Here, we addressed this puzzling observation by analyzing the frequency- and Ca2+-dependence of PPF at unitary PF-to-PN synapses of wild-type (WT) and CR-deficient (CR−/−) mice using paired recordings and computer simulations. Our analysis revealed that PPF in CR−/− is indeed smaller than in the WT, to a degree, however, that indicates that rapid vesicle replenishment and recruitment of additional release sites dominate the synaptic efficacy of the second response. These Ca2+-driven processes operate more effectively in the absence of CR, thereby, explaining the preservation of robust PPF in the mutants.
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