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

TLDR

GABAergic neurons in various brain regions express high levels of parvalbumin, a slow Ca²⁺ buffer that can shape the amplitude and duration of intracellular Ca²⁺ transients in presynaptic terminals and thereby influence short‑term synaptic plasticity. The study aimed to determine whether parvalbumin regulates short‑term plasticity at GABAergic synapses onto Purkinje cells. Paired‑pulse stimulation (30–300 ms intervals) was applied at interneuron–Purkinje cell synapses in wild‑type and parvalbumin‑knockout mice to assess synaptic responses. Paired‑pulse depression occurred in wild‑type mice but was replaced by facilitation in knockouts, and buffering the presynaptic Ca²⁺ with EGTA restored depression, demonstrating that parvalbumin strongly modulates short‑term plasticity.

Abstract

GABAergic (GABA = γ-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.