Article

Glutamatergic synaptic responses and long-term potentiation are impaired in the CA1 hippocampal area of calbindin D(28K)-deficient mice

Università degli Studi di Modena e Reggio Emilia, Modène, Emilia-Romagna, Italy
Synapse (Impact Factor: 2.13). 09/1999; 33(3):172-80. DOI: 10.1002/(SICI)1098-2396(19990901)33:3<172::AID-SYN2>3.0.CO;2-S
Source: PubMed

ABSTRACT

The contribution of the cytosolic calcium binding protein calbindin D(28K) (CaBP) to glutamatergic neurotransmission and synaptic plasticity was investigated in hippocampal CA1 area of wild-type and antisense transgenic CaBP-deficient mice, with the use of extracellular recordings in the ex vivo slice preparation. The amplitude of non-N-methyl-D-aspartate receptor (non-NMDAr)-mediated extracellular field excitatory postsynaptic potentials (fEPSPs) recorded in control medium was significantly greater in CaBP-deficient mice, whereas the afferent fiber volley was not affected. In contrast, the amplitude of NMDAr-mediated fEPSPs isolated in a magnesium-free medium after blockade of non-NMDAr and GABAergic receptors was significantly depressed in these animals. No alteration in the magnitude of paired-pulse facilitation was found, indicating that the presynaptic calcium mechanisms controlling glutamate release were not altered in CaBP-deficient mice. The magnitude and time course of the short-term potentiation (STP) of fEPSPs induced by a 30 Hz conditioning stimulation, which was blocked by the NMDAr antagonist 2-amino-5-phosphonovalerate acid (2-APV), was not impaired in the transgenic mice, whereas long-term potentiation (LTP) induced by a 100 Hz tetanus was not maintained. The long-term depression (LTD) induced by low-frequency stimulation (1 Hz, 15 min) in the presence of the GABA antagonist bicuculline was not altered. These results argue for a contribution of CaBP to the mechanisms responsible for the maintenance of long-term synaptic potentiation, at least in part by modulating the activation of NMDA receptors.

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Available from: Sergio Ferrari, Jan 22, 2014
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    • "Another possibility is calcium induced calcium release from intracellular stores, but it has not been implicated in STP (Carter et al., 2002; Wan et al., 2012). The buffering can be mediated by mitochondria or calcium buffers like calbindin in hippocampal synapses, where the former are implicated in short-term plasticity, but the latter is under debate (Jouvenceau et al., 1999; Wan et al., 2012). The extrusion can be mediated by plasma membrane ATPases (PMCAs) or sodium calcium exchangers, but the latter have low affinity for calcium. "
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    ABSTRACT: Hippocampal neurons show different types of short-term plasticity (STP). Some exhibit facilitation of their synaptic responses and others depression. In this review we discuss presynaptic biophysical properties behind heterogeneity in STP in hippocampal neurons such as alterations in vesicle priming and docking, fusion, neurotransmitter filling and vesicle replenishment. We look into what types of information electrophysiology, imaging and mechanistic models have given about the time scales and relative impact of the different properties on STP with an emphasis on the use of mechanistic models as complementary tools to experimental procedures. Taken together this tells us that it is possible for a multitude of different mechanisms to underlie the same STP pattern, even though some are more important in specific cases, and that mechanistic models can be used to integrate the biophysical properties to see which mechanisms are more important in specific cases of STP.
    Full-text · Article · May 2014 · Frontiers in Cellular Neuroscience
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    • "Moreover, a direct implication of CalB in glutamatergic neurotransmission has been described in the hippocampus. In CalB-deficient mice, N-methyl-D-aspartate (NMDA) receptor-mediated responses were decreased while non-NMDA receptor-mediated responses increased (Jouvenceau et al., 1999). Altogether, these data suggest that CalB may modify amplitude of phase Fig. 3. CalB mRNA expression detected by radioactive in situ hybridization with 35 S-labeled probes on coronal sections at the level of the suprachiasmatic nuclei of hamsters exposed to different photoperiods. "
    Dataset: N2003-122

    Full-text · Dataset · Oct 2012
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    • "Moreover, a direct implication of CalB in glutamatergic neurotransmission has been described in the hippocampus. In CalB-deficient mice, N-methyl-D-aspartate (NMDA) receptor-mediated responses were decreased while non-NMDA receptor-mediated responses increased (Jouvenceau et al., 1999). Altogether, these data suggest that CalB may modify amplitude of phase Fig. 3. CalB mRNA expression detected by radioactive in situ hybridization with 35 S-labeled probes on coronal sections at the level of the suprachiasmatic nuclei of hamsters exposed to different photoperiods. "
    Dataset: N2003-122

    Full-text · Dataset · Oct 2012
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