A use-dependent increase in release sites drives facilitation at calretinin-deficient cerebellar parallel-fiber synapses.
In: Frontiers in Cellular Neuroscience, Jg. 8/9 (2015-02-01), S. 1-11
Online
academicJournal
Zugriff:
Endogenous Ca 2+ -binding proteins affect synaptic transmitter release and short-term plasticity (STP) by buffering presynaptic Ca 2+ 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 Ca 2+ 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 Ca 2+ signals as well as pr. Here, we addressed this puzzling observation by analyzing the frequency- and Ca 2+ -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 Ca 2+ -driven processes operate more effectively in the absence of CR, thereby, explaining the preservation of robust PPF in the mutants. [ABSTRACT FROM AUTHOR]
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Titel: |
A use-dependent increase in release sites drives facilitation at calretinin-deficient cerebellar parallel-fiber synapses.
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Autor/in / Beteiligte Person: | Brachtendorf, Simone ; Eilers, Jens ; Schmidt, Hartmut |
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Zeitschrift: | Frontiers in Cellular Neuroscience, Jg. 8/9 (2015-02-01), S. 1-11 |
Veröffentlichung: | 2015 |
Medientyp: | academicJournal |
ISSN: | 1662-5102 (print) |
DOI: | 10.3389/fncel.2015.00027 |
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