No abstract

Neuronal activity is often associated with changes in gene expression. By a two-dimensional cDNA-display system, restriction landmark cDNA scanning, we identified a novel gene whose expression in the hippocampus was up-regulated by kainate stimulation. The mRNA expression was detected only in brain and up-regulated by the stimulation evoking CA3-CA1 long-term potentiation. The encoded protein contains two copies of C2-domain, known as the Ca P+ -binding domain of PKC-Q Q, and shows 49% identity with human copine I. We designated this protein N-copine (neuronal-copine). N-copine may have a role in synaptic plasticity.z 1998 Federation of European Biochemical Societies.

Bisphenol A (BPA) has been shown to disrupt thyroid hormone function. We therefore studied whether prenatal exposure to low-doses of BPA affects the morphology and the expression of some genes related to brain development in the murine fetal neocortex. Pregnant mice were injected subcutaneously with 20 microg/kg of BPA daily from embryonic day 0 (E0). Control animals received vehicle alone. For evaluating cell proliferation, neuronal differentiation and migration, bromodeoxyuridine (BrdU) was injected intraperitoneally into pregnant mice with various regimens and the brains were processed for immunohistochemistry. The total RNA was extracted from the embryonic telencephalon at various embryonic stages. The BrdU-labeled cells examined 1 hour after BrdU injection showed no differences between the BPA-treated and control groups (n = 10, each), which indicated that the proliferation of precursor cells was not affected. The BrdU-labeled cells, analysed 2 days after BrdU injection, were decreased in the ventricular zone of BPA-treated mice at E14.5 and E16.5, whereas they were increased in the cortical plate at E14.5 as compared with those in control mice (n = 10, each). Furthermore, the expression of Math3, Ngn2, Hes1, LICAM, and THRalpha was significantly upregulated at E14.5 in the BPA-treated group. These results suggested that BPA might disrupt normal neocortical development by accelerating neuronal differentiation/migration.

Bisphenol A (BPA) is an endocrine-disrupting chemical, widely used in various industries and the field of dentistry. The consequent increase in BPA exposure among humans has led us to some concerns regarding the potential deleterious effects on reproduction and brain development. The emphasis of this review is on the effects of prenatal and lactational exposure to low doses of BPA on brain development in mice. We demonstrated that prenatal exposure to BPA affected fetal murine neocortical development by accelerating neuronal differentiation/migration during the early embryonic stage, which was associated with up- and down-regulation of the genes critical for brain development, including the basic helix-loop-helix transcription factors. In the adult mice brains, both abnormal neocortical architecture and abnormal corticothalamic projections persisted in the group exposed to the BPA. Functionally, BPA exposure disturbed murine behavior, accompanied with a disrupted neurotransmitter system, including monoamines, in the postnatal development period and in adult mice. We also demonstrated that epigenetic alterations in promoter-associated CpG islands might underlie some of the effects on brain development after exposure to BPA.

the four cysteines conserved in other chemokines. SCM-1 also Abstract SCM-l/lympbotactin is a chemokine-like molecule produced selectively, if not exclusively, by activated CD8 + T carries a C-terminal sequence 20-30 amino acids longer than cells. Here we report that there are two highly homologous those of other chemokines. Its gene segregated with human SCM-1 genes, which we designate as SCM-la and SCM-I[3.chromosome 1 in somatic hybrid cell lines [3]. Furthermore, Both genes have three exons and two introns. The 1st intron of SCM-1 was found to have a strong sequence similarity to a SCM-la contains a pseudogene of the ribosomal large subunit newly described murine protein lymphotactin (60.5% identity L7a. In SCM-I[J, a 1.5-kb region including about a quarter of at the amino acid level) [4]. Lymphotactin was isolated from a the L7a pseudogene is deleted from the 1st intron. Otherwise, the murine pro-T cell cDNA library, found to be induced in two genes are highly homologous including the 5' and 3' flanking CD8 + T cells and CD4-CD8-thymocytes upon mitogenic regions. Both genes were mapped to human chromosome lq23.stimulations, and shown to be chemotactic for lymphocytes The two genes were similarly induced in peripheral blood but not for monocytes or granulocytes [4]. Subsequently, the mononuclear cells by mitogenic stimulation. Primer extension and RNase protection revealed several transcription initiation human homologue of lymphotactin was isolated and identical sites. The biological activities of SCM-la and SCM-I~, which to SCM-1 [5]. Human lymphotactin was shown to be prohave two amino acid differences at positions 7 and 8 in the duced mainly by activated CD8 + T cells and to induce chemmature proteins, remain to be compared, otactic responses and Ca 2+ flux in lymphocytes but not in monocytes [5].