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

Laboratoire de Physiopharmacologie du Système Nerveux, Paris, France.
Synapse (Impact Factor: 2.43). 09/1999; 33(3):172-80. DOI: 10.1002/(SICI)1098-2396(19990901)33:3<172::AID-SYN2>3.0.CO;2-S
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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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    • "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
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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
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    • "It is interesting to note that immunohistochemical studies have shown that another serotonin receptor subtype, the 5-HT 1A receptor, is colocalized with calbindin in several rat brain regions, including the hippocampus, the thalamus, and the septum (Aznar et al., 2003). As well as modulating photic phase shifts (Hamada et al., 2003), as described above, calbindin has been implicated in several other functions, including spatial memory, long-term potentiation in the hippocampus, synaptic plasticity, and either neuroprotection or enhanced vulnerability to neurodegeneration (Jouvenceau et al., 1999; Chard et al., 1995; Molinari et al., 1996; Nagerl et al., 2000). Some of these functions, such as memory, long-term potentiation, and synaptic plasticity are also modulated by 5-HT 7 receptors (Perez-Garcia and Meneses, 2005; Perez-Garcia et al., 2006; Roberts et al., 2004; Kvachnina et al., 2005). "
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    ABSTRACT: Aging affects several processes modulated by the 5-HT(7) receptor subtype, including circadian rhythms, learning and memory, and depression. Previously, we showed that aging induces a decrease in the hamster dorsal raphe (DRN) in both 5-HT(7) receptor binding and circadian phase resetting responses to 8-OH-DPAT microinjection. To elucidate the mechanisms underlying the aging decrease in 5-HT(7) receptors, we investigated aging modulation of 5-HT(7) receptor mRNA expression in the DRN, brain regions afferent to the DRN, and brain regions regulating circadian rhythms or memory. In situ hybridization for 5-HT(7) receptor mRNA was performed on coronal sections prepared from the brains of young, middle-aged, and old male Syrian hamsters. 5-HT(7) receptor mRNA expression was quantified by densitometry of X-ray film autoradiograms. The results showed that aging did not significantly affect 5-HT(7) receptor mRNA expression in the DRN or most other brain regions examined, with the exception of the cingulate cortex and paraventricular thalamic nucleus. Within the suprachiasmatic nucleus, the site of the master circadian pacemaker in mammals, 5-HT(7) receptor mRNA expression was localized in a discrete subregion resembling the calbindin subnucleus previously described. A second experiment using adjacent tissue sections showed that 5-HT(7) receptor mRNA and calbindin mRNAs were concentrated in the same region of the SCN, and as well as in the same region of several other brain structures. The localization of 5-HT(7) receptors and calbindin mRNAs within the same regions suggests that the proteins they encode may interact to modulate processes such as circadian timekeeping.
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