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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 44 (1995), S. 470-474 
    ISSN: 1420-908X
    Keywords: Mouse ear oedema ; Capsaicin ; Tachyphylaxis ; Substance P ; NK1 receptor antagonist
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined the involvement of substance P (SP) in mouse ear oedema induced by topical application of capsaicin (250 µg/ear). Reapplication of capsaicin at 4h, 24h, and 48h after initial treatment did not induce a second oedema response. Oedema induced after the second application was significantly (p〈0.01 orp〈0.001) suppressed for up to 30 days but was observed when capsaicin was applied 40 days after initial treatment. Topical pretreatment of ears with capsaicin at 4h, 24h and 48h before i.v. injection of SP (5 µg/kg) did not cause a significant inhibition of plasma extravasation in ear skin. NK1 receptor antagonists such as RP 67580 (ED50:0.19 mg/kg, i.v.), spantide II (ED50:0.33 mg/kg, i.v.), and GR 82334 (ED50:0.26 mg/kg, i.v.), inhibited capsaicin-induced ear oedema, whereas SR 48968 (2.0 mg/kg, i.v.), a NK2 receptor antagonist, had no effect. Furthermore, RP 67580 (0.5 kg/mg, i.v.) inhibited the oedema response induced by reapplication of capsaicin at 50 days after initial treatment. These results indicate that tachyphylaxis of capsaicin-induced oedema is reversible and suggest that this response may be due mainly to a reduction of SP in sensory neurones but not to any loss of responsiveness of NK1 receptors. We also conclude that SP and NK1 receptors are involved predominantly in the development of capsaicin-induced mouse ear oedema.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1420-908X
    Keywords: Capsaicin ; Mouse ear oedema ; Tachykinin receptor antagonist ; SR 140333
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined the effect of SR 140333, a nonpeptide NK1 receptor antagonist, FK 888, a peptide NK1 antagonist, and SR 142801, a non-peptide NK3 antagonist, on ear oedema induced by topical application of capsaicin (250 μg/ear) in mice. SR 140333 (ED50: 39 μg/kg, i.v.) dose-dependently inhibited the oedema response to capsaicin, whereas FK 888 (1.0 mg/kg, i.v.) and SR 142801 (3.0 mg/kg, i.v.) had no effect. Furthermore, SR 140333 significantly (p〈0.001) suppressed ear oedema in response to intradermal injection of substance P (SP) (100 pmol/site) by i.v. administration (0.1 mg/kg), and co-injection (50 pmol/site). In contrast, FK 888 (1.0 mg/kg, i.v. and 500 pmol/site) was ineffective in the response to SP. The present results suggest that the difference in effects of the two NK1 receptor antagonists on the oedema response to capsaicin is due to species differences in affinities for the NK1 receptor in the mouse skin. Moreover, it seems unlikely that the NK3 receptor is involved primarily in capsaicin-induced mouse ear oedema.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Current genetics 37 (2000), S. 119-124 
    ISSN: 1432-0983
    Keywords: Key words Ribosomal protein gene crp-7 ; RFLP mapping ; Super induction ; Neurospora crassa
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract We have isolated and characterized a Neurospora crassa cytoplasmic ribosomal protein gene, named crp-7, which is found upstream of the photolyase gene. The deduced amino-acid sequence of this gene is highly homologous to the YS25 ribosomal protein of Saccharomyces cerevisiae. The crp-7 ORF consists of two exons which are separated by a short intron. The deduced polypeptide contains 87 amino acid residues and has a calculated molecular weight of 9.7 kDa. RFLP mapping showed that the crp-7 gene is located on the right arm of linkage group I. Southern blot hybridization analyses indicated that there is only one copy of the crp-7 gene in the N. crassa genome. Transcriptional elements, the Dde box, the Taq box and the CG element, that have been identified in other N. crassa ribosomal protein genes are observed in the promoter region of the crp-7 gene. The crp-7 mRNA levels were low in conidia and highest in young mycelia during vegetative growth. The mRNA levels of four r-protein genes, including the crp-7 gene, as well as the tef-1 gene encoding translational elongation factor 1α, were raised following the treatment of mycelia with a low concentration of cycloheximide. This indicates that the expression of r-protein genes is under the control of so-called super-induction.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Mutation Research/DNA Repair 218 (1989), S. 95-103 
    ISSN: 0921-8777
    Keywords: DNA repair ; Neurospora crassa ; Photoreactivation ; Reversion ; UV sensitivity
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Mutation Research/DNA Repair 315 (1994), S. 249-259 
    ISSN: 0921-8777
    Keywords: DNA repair ; Meiotic mutant ; Mutator ; Neurospora crassa ; Recombination repair
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1617-4623
    Keywords: Key wordslah-1 ; cpc-1 ; Laccase ; Cycloheximide-inducible genes ; Neurospora crassa
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract In Neurospora crassa, expression of the laccase gene is induced by treatment with the protein synthesis inhibitor cycloheximide (CHX). This expression is mediated by CPC1, which acts as a general transcriptional activator when mycelia are treated with CHX or starved for any one of the amino acids. A laccase-derepressed mutant, lah-1, shows pleiotropic deficiencies in growth, hyphal morphology, CHX sensitivity, and production of protoperithecia. Moreover, in the lah-1 mutant, transcript levels of CHX-inducible genes, including lacc, tub-2, tef-1, and amino acid biosynthetic genes such as cpc-1, trp-3, and arg-12, are increased without exposure to CHX. All of the defects exhibited in the lah-1 mutant are suppressed by a mutation in the cpc-1 locus. These findings suggest that the cpc-1 mutation is epistatic to the lah-1 mutation and that the pleiotropic defects in the lah-1 mutant are attributable to constitutive expression of CPC1. These conclusions are supported by a developmental Northern blot analysis of the CHX-inducible genes. Based on these results, the lah-1 gene product appears to regulate expression of the cpc-1 gene negatively. Expression of the CHX-inducible genes was induced by CHX treatment in the lah-1 cpc-1 mutant, as well as in the cpc-1 mutant. This observation indicates that LAH1 is not a component of CHX-responsive pathway itself.
    Type of Medium: Electronic Resource
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