Developmental Changes in Parvalbumin Regulate Presynaptic Ca²⁺Signaling

Visual thalamocortical circuits in parvalbumin-deficient mice

“…Also, in striatal fast-spiking interneurons of PVKO mice, the increased excitability is reverted close to the WT situation by adding EGTA to the patch pipette (Orduz et al, in press). Furthermore, PV expression in the mouse brain starts relatively late commencing between postnatal day 10 (P10) and P14 as evidenced in the neocortex (del Río et al, 1994) and in the cerebellum (Collin et al, 2005); not surprisingly, no principal differences in the distribution and morphology of "PV-ir" neurons in PVKO mice are observed, neither in the hippocampus (Vreugdenhil et al, 2003) nor the cortex (Schwaller et al, 2004). All these results strongly support our hypothesis that changes observed in PVKO mice are mostly the direct result of PV's absence, rather than caused by compensation mechanisms in these mice.…”

“…PV is characterized by a slow-onset Ca 2+ binding that generally does not affect the initial amplitude of Ca 2+ transients, but then accelerates the decay phase, thus often converting a monoexponential [Ca 2+ ] i decay into a bi-exponential one n (Collin et al, 2005;Lee et al, 2000). The acceleration of the early phase of [Ca 2+ ] i decay associated to PV activity limits or slows down the buildup of residual [Ca 2+ ] i in presynaptic terminals, thus affecting short-term plasticity (Caillard et al, 2000;Vreugdenhil et al, 2003).…”

Differences in locomotor behavior revealed in mice deficient for the calcium-binding proteins parvalbumin, calbindin D-28k or both

“…Closer inspection of PV−/−, CB−/− and PV−/−CB−/− mice revealed significant functional alterations at cortical, hippocampal and cerebellar levels (for a review on the cerebellum, see [4]). Electrophysiological recordings of cortical, hippocampal and cerebellar sites in PV−/− mice showed important modifications in the function of the inhibitory systems [14,16,17,35]. Moreover, direct evidence that endogenous CaBPs play an important role in the cerebellar physiology was provided by behavioral analysis investigated in CB−/− mice and more recently in mice lacking the closely related protein calretinin.…”

“…Previous work reported several physiological alterations at neuronal and muscular levels in these animals. PV−/− mice revealed electrophysiological alterations associated with PV-expressing cortical neurons [14], cerebellar stellate and basket cells [15,16] and hippocampal PV-immunoreactive interneurons [17]. CB−/− mice showed impairment in motor coordination associated with altered synaptic Ca 2+ transients in Purkinje cell dendrites [12].…”

Cytosolic Ca2+ Buffers

“…The concentration of PV is as high as 1.5 mM in the superfast swimbladder muscle of toadfish (Tikunov and Rome 2009) and approximately 1 mM in mouse fast-twitch muscle, while it is lower in other muscles and highly correlated with the speed of muscle relaxation (Heizmann et al 1982). Within different neuron subpopulations, PV is on average one order of magnitude lower (50 -150 mM): 80 mM in mouse (Schmidt et al 2003b) and 120 mM in rat (Hackney et al 2005) Purkinje cells; 150 mM in mouse cerebellar interneurons (Collin et al 2005), and 100 -300 mM in inner and outer hair cells from inner ear (Hackney et al 2005). The concentration of mammalian b PV called oncomodulin (OM) is particularly high in rat cochlear outer hair cells (2-3 mM) (Hackney et al 2005).…”