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Trisomy 21 (Down syndrome, DS) is the most common human genetic anomaly associated with heart defects. Based on evolutionary conservation, DS-associated heart defects have been modeled in mice. By generating and analyzing mouse mutants carrying different genomic rearrangements in human chromosome 21 (Hsa21) syntenic regions, we found the triplication of the(More)
We have previously shown that glycine binding sites on presynaptic NMDA receptors (NMDA-Rs) can tonically regulate glutamate release in the rat visual cortex. In the present study, we investigated the subunit composition of these presynaptic NMDA-Rs. We recorded miniature a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated(More)
Trisomy 21 (Down syndrome, DS) is the most common genetic cause of developmental cognitive deficits, and the so-called Down syndrome critical region (DSCR) has been proposed as a major determinant of this phenotype. The regions on human chromosome 21 (Hsa21) are syntenically conserved on mouse chromosome 10 (Mmu10), Mmu16 and Mmu17. DSCR is conserved(More)
A polymerase chain reaction (PCR) assay was performed in this study to amplify the major surface protein 5 (msp5) gene from the genomic DNA of Anaplasma marginale in Hyalomma asiaticum ticks by species-specific primers. Sequence analysis showed that the msp5 gene was 643 bases long and that the PCR products from the samples had an identical sequence(More)
To investigate the effects of a dietary antibiotic growth promoter (florfenicol) and a Saccharomyces cerevisiae fermentation product (DVAQUA) on growth, G:F, daily feed intake, intestinal bacterial community, and nonspecific immunity of hybrid tilapia (Oreochromis niloticus ♀ × Oreochromis aureus ♂), a 16-wk feeding trial was conducted in a recirculating(More)
Down syndrome (DS), caused by trisomy 21, is the most common chromosomal disorder associated with developmental cognitive deficits. Despite intensive efforts, the genetic mechanisms underlying developmental cognitive deficits remain poorly understood, and no treatment has been proven effective. The previous mouse-based experiments suggest that the so-called(More)
Activity-dependent structural plasticity of dendritic spines of pyramidal neurons in the central neuron system has been proposed to be a cellular basis of learning and memory. Long-term potentiation (LTP) is accompanied by changes in synaptic morphology and structural remodeling of dendritic spines. However, there is considerable uncertainty as to the(More)
A large variability of paired-pulse plasticity (PPP) has been reported in CA3-CA1 synapses, and paired-pulse facilitation (PPF) has long been extensively used as a relative index of release probability (P(r)) from the presynaptic terminal. One of the most common ways of studying P(r) and PPP is to pass paired-pulse stimulation (PPS) through an electrode to(More)
Long-term potentiation (LTP) is a well-characterized form of synaptic plasticity that fulfills many of the criteria for the neural correlate of memory. LTP reversal (or depotentiation, DP) is thought to correlate with prevention or elimination of memory storage. LTP during and immediately after induction can be easily reversed by afferent stimulation, when(More)