Toward Open-Closed String Theoretical Description of Rolling Tachyon

We consider how the time-dependent decay process of an unstable D-brane should be described in the full (quantum) open-closed string theory. It is argued that the system, starting from the unstable D-brane configuration, will evolve in time into the time-independent open string tachyon vacuum configuration which we assume to be finite, with the total energy conserved. As a concrete realization of this idea, we construct a toy model describing the open and closed string tachyons which admits such a time-dependent solution. The structure of our model has some resemblance to that of open-closed string field theory.Comment: 1+10 pages, 6 figures. v2: a reference adde

Required Elements in tRNA for Methylation by the Eukaryotic tRNA (Guanine-N2-) Methyltransferase (Trm11-Trm112 Complex)

The Saccharomyces cerevisiae Trm11 and Trm112 complex (Trm11-Trm112) methylates the 2-amino group of guanosine at position 10 in tRNA and forms N2-methylguanosine. To determine the elements required in tRNA for methylation by Trm11-Trm112, we prepared 60 tRNA transcript variants and tested them for methylation by Trm11-Trm112. The results show that the precursor tRNA is not a substrate for Trm11-Trm112. Furthermore, the CCA terminus is essential for methylation by Trm11-Trm112, and Trm11-Trm112 also only methylates tRNAs with a regular-size variable region. In addition, the G10-C25 base pair is required for methylation by Trm11-Trm112. The data also demonstrated that Trm11-Trm112 recognizes the anticodon-loop and that U38 in tRNAAla acts negatively in terms of methylation. Likewise, the U32-A38 base pair in tRNACys negatively affects methylation. The only exception in our in vitro study was tRNAValAAC1. Our experiments showed that the tRNAValAAC1 transcript was slowly methylated by Trm11-Trm112. However, position 10 in this tRNA was reported to be unmodified G. We purified tRNAValAAC1 from wild-type and trm11 gene deletion strains and confirmed that a portion of tRNAValAAC1 is methylated by Trm11-Trm112 in S. cerevisiae. Thus, our study explains the m2G10 modification pattern of all S. cerevisiae class I tRNAs and elucidates the Trm11-Trm112 binding sites

On Ghost Structure of Vacuum Superstring Field Theory

After discussing the general form of the kinetic operator around the tachyon vacuum, we determine the specific form of the pure-ghost kinetic operator Q^ by requiring the twist invariance of the action. We obtain a novel result that the Grassmann-even piece Q_even of Q^ must act differently on GSO(+) sector and on GSO(-) sector to preserve the twist invariance, and show that this structure is crucial for gauge invariance of the action. With this choice of Q^, we construct a solution in an approximation scheme which is conjectured to correspond to a non-BPS D9-brane. We consider both 0-picture cubic and Berkovits' non-polynomial superstring field theories for the NS sector.Comment: 1+42 pages, 5 figures. v2: a reference added, and a brief comment added (footnote 14). v3: version to appear in NPB. Numerical coefficients in front of the kinetic operators, and some signs in the eqs. of motion, have been corrected. Some minor modification

Comments on Solutions of Vacuum Superstring Field Theory

We study classical solutions of vacuum version of Berkovits' superstring field theory, focusing on the (super)ghost sector. We first argue that the supersliver state which is annihilated by eta_0, though it has the correct quantum numbers and solves the equation of motion, is actually non-perturbatively pure-gauge, and hence it fails to describe a D-brane. As a step toward the construction of non-trivial solutions, we calculate e^{-Phi}Qe^{Phi} for twisted superslivers. As a by-product, we find that the bc-twisted sliver solution in bosonic VSFT can, at least formally, also be written as a pure-gauge configuration.Comment: 1+21 pages, no figures. v2:Some expressions in eqs.(4.11)-(5.4) have been corrected, with our main conclusions unchange

Repeated Exposure to Methamphetamine, Cocaine or Morphine Induces Augmentation of Dopamine Release in Rat Mesocorticolimbic Slice Co-Cultures

Repeated intermittent exposure to psychostimulants and morphine leads to progressive augmentation of its locomotor activating effects in rodents. Accumulating evidence suggests the critical involvement of the mesocorticolimbic dopaminergic neurons, which project from the ventral tegmental area to the nucleus accumbens and the medial prefrontal cortex, in the behavioral sensitization. Here, we examined the acute and chronic effects of psychostimulants and morphine on dopamine release in a reconstructed mesocorticolimbic system comprised of a rat triple organotypic slice co-culture of the ventral tegmental area, nucleus accumbens and medial prefrontal cortex regions. Tyrosine hydroxylase-positive cell bodies were localized in the ventral tegmental area, and their neurites projected to the nucleus accumbens and medial prefrontal cortex regions. Acute treatment with methamphetamine (0.1–1000 µM), cocaine (0.1–300 µM) or morphine (0.1–100 µM) for 30 min increased extracellular dopamine levels in a concentration-dependent manner, while 3,4-methylenedioxyamphetamine (0.1–1000 µM) had little effect. Following repeated exposure to methamphetamine (10 µM) for 30 min every day for 6 days, the dopamine release gradually increased during the 30-min treatment. The augmentation of dopamine release was maintained even after the withdrawal of methamphetamine for 7 days. Similar augmentation was observed by repeated exposure to cocaine (1–300 µM) or morphine (10 and 100 µM). Furthermore, methamphetamine-induced augmentation of dopamine release was prevented by an NMDA receptor antagonist, MK-801 (10 µM), and was not observed in double slice co-cultures that excluded the medial prefrontal cortex slice. These results suggest that repeated psychostimulant- or morphine-induced augmentation of dopamine release, i.e. dopaminergic sensitization, was reproduced in a rat triple organotypic slice co-cultures. In addition, the slice co-culture system revealed that the NMDA receptors and the medial prefrontal cortex play an essential role in the dopaminergic sensitization. This in vitro sensitization model provides a unique approach for studying mechanisms underlying behavioral sensitization to drugs of abuse