Folia Pharmacologica Japonica
Online ISSN : 1347-8397
Print ISSN : 0015-5691
ISSN-L : 0015-5691
Volume 110, Issue 4
Displaying 1-7 of 7 articles from this issue
  • Yosuke TOJYO, Akihiko TANIMURA, Yoshito MATSUMOTO
    1997 Volume 110 Issue 4 Pages 163-172
    Published: 1997
    Released on J-STAGE: September 07, 2011
    JOURNAL FREE ACCESS
    The capacitative Ca2+ entry has been accepted to play a crucial role in Ca2+ signaling in nonexcitable cells, and the mechanisms linking the depletion of intracellular Ca2+ to the activation of Ca2+ entry are presently the subject of intensive investigation. There are two hypotheses to explain the molecular mechanism of capacitative Ca2 entry. One is that a diffusible second messenger released from intracellular Ca2+ stores may activate a Ca 2+ channel at the plasma membrane. Numerous molecules, including CIF, cGMP, arachidonic acid, and a small G-protein, are proposed as the candidates for the diffusible messenger. In addition, the capacitative Ca2+ entry has been suggested to be modulated by protein phosphorylation/ dephosphorylation. Another hypothesis is termed the “conformational coupling model”. This model suggests that information between the IP3 receptor and a plasma membrane Ca2+ channel may be transferred directly through conformational protein-protein interactions. The plasma membrane Ca2+ involved in the capacitative Ca2+ entry is still neither purified nor cloned, but recent studies suggest that the mammalian homologue of the Drosophila protein Trp may function as a capacitative Ca2+ entry channel.
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  • Kazuhide INOUE
    1997 Volume 110 Issue 4 Pages 173-182
    Published: 1997
    Released on J-STAGE: September 07, 2011
    JOURNAL FREE ACCESS
    ATP receptors in the central nervous system (CNS) are divided into 2 major classes, ionotropic (P2Xn) and G protein-coupled (P2Yn) ATP receptors. P2Xn receptors, a member of the 2-transmembrane family, contain non-selective cation channels that may play a role in rapid synaptic transmission. Seven subtypes of P2Xn were reported so far. Although all of these subtypes are distributed in the CNS, P2X4 and P2X6 are most abundantly and widely distributed. P2X3 is distributed only in trigeminal ganglia neurons as well as in small-diameter DRG neurons, suggesting their relation to pain. P2Yn receptors, a member of the 7-transmembrane superfamily, are coupled with Gq/11 to activate PLCβ. These receptors are thought to play an important role in the modulation of synaptic efficacy. Seven subtypes of P2Yn were reported so far. P2Y1, P2Y2, P2Y3 and P2Y4 are distributed in the CNS. Neither selective agonists nor antagonists to P2Xn and P2Yn are known.
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  • Toyoaki HAYAMA
    1997 Volume 110 Issue 4 Pages 183-193
    Published: 1997
    Released on J-STAGE: September 07, 2011
    JOURNAL FREE ACCESS
    In this review, I will describe honybee biology from my prospective as a veterinary pharmacologist and will provide a summary of my research project to search for effective drugs to control American foulbrood, a bacterial disease of honeybees. In conclusion, mirosamicin, a macrolide antibiotic, as a preventive and glutaral, an alkylating agent, as a disinfectant were the most promising drugs.
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  • Minako HASHII, Haruhiro HIGASHIDA
    1997 Volume 110 Issue 4 Pages 195-203
    Published: 1997
    Released on J-STAGE: September 07, 2011
    JOURNAL FREE ACCESS
    Signal transduction from mouse bradykinin B2-receptors to Ca2+ influx was studied in single control or v-Ki-ras-transformed NIH/3T3 (DT) fibroblasts. Microspectrofluometry (fura-2) was combined with the whole-cell patch-clamp technique to study bradykinin-activated Ca2+ influx. Cytosolic Ca2+ oscillations observed at holding potentials of-20 to-80 mV were terminated by holding at-10 mV or more depolarized potentials. Bradykinin significantly enhanced the hyperpolarization-induced increases in the intracellular free Ca2+ concentration upon membrane hyperpolarization only in DT cells but not in control cells. Internal application of 10 μM inositol 1, 3, 4, 5-tetrakisphosphate (InsP4) mimicked membrane potential-dependent Ca2+ entry. Activation of B2-receptors resulted in a decrease of cellular fluorescence at the excitation wavelength of 340 or 360 nm after MnCl2 application in DT cells. This Mn2+ entry through the Ca2+ influx pathway increased with membrane hyperpolarization below-20 mV. The results suggest that bradykinininduced cytosolic Ca2+ oscillations in ras-transformed NIH/3T3 cells are maintained by bradykinin-activated continuous Ca2+ influx, which may use Ins (1, 3, 4, 5) P4 as an intracellular messenger.
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  • Kenroh SASAKI, Masaru MIYAKAWA, Teppei SUDO, Fumihiko YOSHIZAKI
    1997 Volume 110 Issue 4 Pages 205-213
    Published: 1997
    Released on J-STAGE: September 07, 2011
    JOURNAL FREE ACCESS
    Evaluation of marble burying behavior (MBB) housing-induced alteration of monoamine metabolism in mouse brain was performed by measuring metabolite levels with HPLC-ECD. Isolated housing of mice, each in a cage (22 × 32 × 14 cm; sawdust, 1-mm diameter; 5 cm in thickness) with 15 evenly spaced glass marbles on the floor (2.5-cm diameter; control, without marbles) for 24-168 hr, 5-HIAA contents were decreased in three regions : the midbrain, thalamus and hypothalamus. 5-HT turnover was not inhibited except for in the hypothalamus due to the decreases of 5-HT in the other two regions. On the other hand, DOPAC content and DA turnover were decreased in four regions : striatum, midbrain, thalamus, hypothalamus. The decrease in hypothalamic monoamine neurons was observed notably after 72 hr of MBB housing. No alterations were observed in feeding, water-drinking, spontaneous locomotor activity, number of buried marbles, serum corticosterone and serum glucose concentrations during MBB keeping compared with the control mice. These results suggested that the isolated mouse housed in a cage with evenly spaced glass marbles for a long period may be a model animal for alteration of monoamine metabolism in brain regions without physical infringement.
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  • 1997 Volume 110 Issue 4 Pages b63-b82
    Published: 1997
    Released on J-STAGE: September 07, 2011
    JOURNAL FREE ACCESS
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  • 1997 Volume 110 Issue 4 Pages b83-b106
    Published: 1997
    Released on J-STAGE: September 07, 2011
    JOURNAL FREE ACCESS
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