16 research outputs found

    Properties of the Disorder Induced in the Purple Membrane Structure by Iodination

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    Iodination induces disorder in the crystalline structure of purple membrane. The properties Of the disorder were examined by X-ray diffraction experiments on the iodinated purple membrane. The analysis of the intensity and the integral width of the Bragg reflections revealed that the disorder was well characterized by the second kind of disorder. The g value, which represents the extent of the second kind of disorder, is obtained for iodinated purple membrane with various extent of iodination. The g value and the wavelength at absorption maximum of iodinated PM are well correlated, indicating that the local change around retinal is reflected in the disorder in the crystalline structure of purple membrane

    A Marking Method for Kuruma Prawn <i>Penaeus japonicus</i>

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    Acute and late effects on induction of allodynia by acromelic acid, a mushroom poison related structurally to kainic acid

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    1. Ingestion of a poisonous mushroom Clitocybe acromelalga is known to cause severe tactile pain (allodynia) in the extremities for a month and acromelic acid (ACRO), a kainate analogue isolated from the mushroom, produces selective damage of interneurons of the rat lower spinal cord when injected either systemically or intrathecally. Since ACRO has two isomers, ACRO-A and ACRO-B, here we examined their acute and late effects on induction of allodynia. 2. Intrathecal administration of ACRO-A and ACRO-B provoked marked allodynia by the first stimulus 5 min after injection, which lasted over the 50-min experimental period. Dose-dependency of the acute effect of ACRO-A on induction of allodynia showed a bell-shaped pattern from 50 ag kg(−1) to 0.5 pg kg(−1) and the maximum effect was observed at 50 fg kg(−1). On the other hand, ACRO-B induced allodynia in a dose-dependent manner from 50 pg kg(−1) to 50 ng kg(−1). 3. N-methyl-D-aspartate (NMDA) receptor antagonists and Joro spider toxin, a Ca(2+)-permeable AMPA receptor antagonist, inhibited the allodynia induced by ACRO-A, but not by ACRO-B. However, other AMPA/kainate antagonists did not affect the allodynia induced by ACRO. 4. Whereas no neuronal damage was observed in the spinal cord in ACRO-A-treated mice, induction of allodynia by ACRO-A (50 fg kg(−1)) and ACRO-B (50 ng kg(−1)) was selectively lost 1 week after i.t. injection of a sublethal dose of ACRO-A (50 ng kg(−1)) or ACRO-B (250 ng kg(−1)). Higher doses of ACRO-A, however, could evoke allodynia dose-dependently from 50 pg kg(−1) to 500 ng kg(−1) in the ACRO-A-treated mice. The allodynia induced by ACRO-A (500 ng kg(−1)) was not inhibited by Joro spider toxin or NMDA receptor antagonists. These properties of the late allodynia induced by ACRO-A were quite similar to those of the acute allodynia induced by ACRO-B. 5. ACRO-A could increase [Ca(2+)](i) in the deeper laminae, rather than in the superficial laminae, of the spinal cord. This increase was not blocked by the AMPA-preferring antagonist GYKI52466 and Joro spider toxin. 6. Taken together, these results demonstrate the stereospecificity of ACRO for the induction of allodynia and suggest the presence of a receptor specific to ACRO
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