In: The Journal of Neuroscience, 2007, vol. 27, no. 9, p. 2261-2271
Presynaptic Ca²⁺ signaling plays a crucial role in short-term plasticity of synaptic transmission. Here, we studied the role of mobile endogenous presynaptic Ca²⁺ buffer(s) in modulating paired-pulse facilitation at a large excitatory nerve terminal in the auditory brainstem, the calyx of Held. To do so, we assessed the effect of presynaptic whole-cell recording, which should lead to the...
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In: Behavioural Brain Research, 2007, vol. 178, no. 2, p. 250-261
We investigated the role of the two calcium-binding proteins parvalbumin (PV) and calbindin D-28k (CB) in the locomotor activity and motor coordination using null-mutant mice for PV (PV−/−), CB (CB−/−) or both proteins (PV−/−CB−/−). These proteins are expressed in distinct, mainly non-overlapping populations of neurons of the central and peripheral nervous system and PV...
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In: Journal of Neurochemistry, 2007, vol. 100, no. 3, p. 727–735
The Ca²⁺-binding protein (CaBP) parvalbumin (PV) is strongly expressed in cerebellar Purkinje neurones (PNs). It is considered a pure Ca²⁺ buffer, lacking any Ca²⁺ sensor function. Consistent with this notion, no PV ligand was found in dendrites of PNs. Recently, however, we observed for a related CaBP that ligand-targeting differs substantially between dendrites and axons. Thus, here we...
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In: Neuroscience, 2006, vol. 142, no. 1, p. 97-105
The Ca²⁺-binding proteins parvalbumin (PV) and calbindin D-28k (CB) are key players in the intracellular Ca²⁺-buffering in specific cells including neurons and have profound effects on spatiotemporal aspects of Ca²⁺ transients. The previously observed increase in mitochondrial volume density in fast-twitch muscle of PV−/− mice is viewed as a specific compensation mechanism to...
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In: FEBS Journal, 2006, vol. 273, no. 1, p. 96-108
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In: Experimental Neurology, 2004, vol. 186, no. 1, p. 78-88
A neuroprotective role for Ca²⁺-binding proteins in neurodegenerative conditions ranging from ischemia to Alzheimer's disease has been suggested in several studies. A key phenomenon in neurodegeneration is the Ca²⁺-mediated excitotoxicity brought about by the neurotransmitter glutamate. To evaluate the relative ability to resist excitotoxicity of neurons containing the slow-onset...
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In: Neuroscience, 2004, vol. 123(2), p. 459-466
Following nerve injury in neonatal rats, a large proportion of motoneurons die, possibly as a consequence of an increase in vulnerability to the excitotoxic effects of glutamate. Calcium-dependent glutamate excitotoxicity is thought to play a significant role not only in injury-induced motoneuron death, but also in motoneuron degeneration in diseases such as amyotrophic lateral sclerosis (ALS)....
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In: Cell Calcium, 2005, vol. 37, no. 3, p. 233-243
Antisense oligodeoxynucleotides (AS-ODNs) were used in combination with transient functional expression of the cardiac Na⁺–Ca²⁺ exchanger (NCX1) to correlate suppression of the Na⁺–Ca²⁺ exchange function with down-regulation of NCX1 protein expression. In a de-novo expression system (Sf9 cells), a decrease in both, NCX1 mRNA and protein after AS-ODN application was paralleled by...
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In: The Journal of Neuroscience, 2005, vol. 25, no. 1, p. 96-107
Certain interneurons contain large concentrations of specific Ca²⁺-binding proteins (CBPs), but consequences on presynaptic Ca²⁺ signaling are poorly understood. Here we show that expression of the slow CBP parvalbumin (PV) in cerebellar interneurons is cell specific and developmentally regulated, leading to characteristic changes in presynaptic Ca²⁺ dynamics (Cai). Using...
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In: Molecular and Cellular Neuroscience, 2004, vol. 25, no. 4, p. 650-663
Networks of GABAergic interneurons are of utmost importance in generating and promoting synchronous activity and are involved in producing coherent oscillations. These neurons are characterized by their fast-spiking rate and by the expression of the Ca2+-binding protein parvalbumin (PV). Alteration of their inhibitory activity has been proposed as a major mechanism leading to epileptic seizures...
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