Abstract. We report here that all trans-retinoic acid (RA), a classical morphogen, induces apoptosis during the neural differentiation of the embryonic stem cell line P19. The apoptotic cells showed, in addition to DNA cleavage, typical morphological changes including chromatin condensation, nuclear fragmentation, and cytoplasmic vacuolation. These apoptotic changes became obvious by 12 h after the addition of RA. The endogenous expression of bcl-2 in surviving cells was down-regulated during this process, and the compelled expression of bcl-2 by retroviral vectors reduced the number of apoptotic cells. Apoptosis was partially inhibited by adding antisense oligonucleotides against RA receptors (RARs) simultaneously or by transfecting a plasmid vector flanked with a RA-responsive element. Antisense oligonucleotides against retinoid X receptors (RXRs), the receptors for 9 cis-RA, did not inhibit apoptosis indUced by all trans-RA. Cycloheximide and actinomycin D, inhibitors of protein and RNA syntheses, respectively, suppressed apoptosis. No changes were seen in the expression of tumor necrosis factors, their receptors, Fas, FasL, p53, or c-myc, molecules which have been suggested to participate in the apoptotic process. Addition of neurotrophins to the culture medium did not affect apoptosis. These findings suggest that the signals mediated by RARs, the differentiation signals themselves, promote expression of molecules essential for apoptosis. Furthermore, we observed that RA induced apoptosis of cerebral neurons from murine embryos in primary culture, which suggests that RA might participate in cell death which occurs during neural development.OPTOSIS is a biological process which causes programmed cell death during development and may participate in various pathological processes. It is characterized by typical morphological changes including chromatin condensation, nuclear fragmentation, cytoplasmic vacuolation, membrane blebbing and cell shrinkage, as well as by the biochemical marker DNA cleavage. Apoptosis eliminates 20-80% of neurons during development (Hamburger and Oppenheim, 1982;Oppenheim, 1991) but leaves neurons which are indispensable for the function of the nervous system. This process seems essential because unnecessary neurons might disturb the development of neural networks. The apoptotic process is also observed under conditions stressful for neurons such as serum/neurotrophic factor deprivation (Greene and Tischer, Address all correspondence to H. Okazawa,
We investigated tile effect of dopamine on the m wvo expression of brain-derived ncurotrophic factor (BDNF) ill tile ~tnatum of mouse. BDNF mRNA ~xpre~sion in the ~triatum, which wa~ quantified with the rever~e tranbcnpta~e polymerase chain reaction, was up-regulated from 2 h after oraladrnmistrationoflevodopa, a precursorofdopamme. Theincreasewa~ustain~.~d for 16h Co.admm~strationofhalope~idotpartmllymh:bited dopamiae-mduced BDNF enhancement. The~e data ~ug~cst that dop,tminergic stimulatton diiectly promotes the exptension of BDNF in the striatttm in wvo, Brain-derived neurotrophic factor; Dopamme; Tr,mscnption, Stnatuln
We have successfully observed two-photon above-threshold ionization in rare gas atoms (Ar, Xe, and He) by the fifth harmonic (25 eV photon energy) of a KrF laser. Use of the energy-resolved photoelectron counting system together with our laser, providing strong 25 eV radiation at 40-100 Hz, enabled us to detect the very weak single-color two-photon above-threshold ionization signals. Experimental data are in good agreement with our theoretical calculations newly developed along the line of multichannel quantum defect theory.
A series of bis(&mgr;-oxo)dirhenium complexes, [Re(2)(&mgr;-O)(2)(L)(2)](PF(6))(n)() (L = tris(2-pyridylmethyl)amine (tpa), n = 3 (1), n = 4 (1a); L = ((6-methyl-2-pyridyl)methyl)bis(2-pyridylmethyl)amine (Metpa), n = 3 (2), n = 4 (2a); bis((6-methyl-2-pyridyl)methyl)(2-pyridylmethyl)amine (Me(2)tpa), n = 3 (3), n = 4 (3a)), have been prepared and characterized by several physical methods. X-ray crystallographic studies for 2, 2a.2CH(3)CN.2H(2)O (2a'), and 3a' (ReO(4)(-) salt), include the first structural determinations of (i) the bis(&mgr;-oxo)-Re(III)Re(IV) complex (2) and (ii) the pair of Re(III)Re(IV) and Re(IV)(2) complexes (2 and 2a'). All the complexes have a centrosymmetric structure, suggesting that the mixed-valence state 2 is of structurally delocalized type. The Re-Re distances for 2, 2a.2CH(3)CN.2H(2)O, and 3a' are 2.426(1), 2.368(1), and 2.383(1) Å, respectively, being consistent with the bond order of 2.5 (sigma(2)pi(2)delta(2)delta) for 2 and 3 (sigma(2)pi(2)delta(2)) for the others. Methyl substitution on the pyridyl moiety of the ligands has no significant influence to the overall structure. Cyclic voltammetry of 1 shows two reversible redox waves at -0.77 ((III,III)/(III,IV)) and 0.09 V ((III,IV)/(IV,IV)) vs Ag/AgCl in acetonitrile. The potentials are slightly more positive for 2 (-0.66 and 0.14 V) and 3(-0.64 and 0.20 V). No proton-coupled redox behavior was observed on addition of p-toluenesulfonic acid. Complexes, 1a, 2a, and 3a show a strong visible absorption band at 477 nm (epsilon, 9200 dm(3) mol(-)(1) cm(-)(1)), 482 (11200), and 485 (8700), respectively, which is assigned to the pi-pi transition within the Re(2)(&mgr;-O)(2) core. For the mixed-valence complexes 1, 2, and 3, a strong band is observed in the longer wavelength region (556-572 nm). Crystal data: 2, monoclinic, space group C2/c (No.15), a = 11.799(2) Å, b = 19.457(3) Å, c = 21.742(4) Å, beta = 98.97(1) degrees, Z = 4; 2a', triclinic, space group P&onemacr; (No. 2), a = 13.151(3) Å, b = 13.535(2) Å, c = 10.243(3) Å, alpha = 104.37(2) degrees, beta = 109.02(2) degrees, gamma = 106.87(1) degrees, Z = 1; 3a', monoclinic, space group P2(1)/n (No. 14), a = 13.384(3) Å, b = 14.243(2) Å, c = 13.215(6) Å, beta = 106.88(2) degrees, Z = 2.
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