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Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):13372-7.

Role of the calcium-binding protein parvalbumin in short-term synaptic plasticity.

Author information

1
Max-Planck-Institute for Biophysical Chemistry, D37 077 Göttingen, Germany. caillard@luminy.univ-mrs.fr

Abstract

GABAergic (GABA = gamma-aminobutyric acid) neurons from different brain regions contain high levels of parvalbumin, both in their soma and in their neurites. Parvalbumin is a slow Ca(2+) buffer that may affect the amplitude and time course of intracellular Ca(2+) transients in terminals after an action potential, and hence may regulate short-term synaptic plasticity. To test this possibility, we have applied paired-pulse stimulations (with 30- to 300-ms intervals) at GABAergic synapses between interneurons and Purkinje cells, both in wild-type (PV+/+) mice and in parvalbumin knockout (PV-/-) mice. We observed paired-pulse depression in PV+/+ mice, but paired-pulse facilitation in PV-/- mice. In paired recordings of connected interneuron-Purkinje cells, dialysis of the presynaptic interneuron with the slow Ca(2+) buffer EGTA (1 mM) rescues paired-pulse depression in PV-/- mice. These data show that parvalbumin potently modulates short-term synaptic plasticity.

PMID:
11069288
PMCID:
PMC27231
DOI:
10.1073/pnas.230362997
[Indexed for MEDLINE]
Free PMC Article

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