Machiko Watanabe

Inhibition of adjuvant-induced inflammatory hyperalgesia in rats by local injection of neurotrophin-3.

The induction of nerve growth factor (NGF) in inflammatory tissue has been shown to be involved in hyperalgesia. In the present study, the role of neurotrophin-3 (NT-3) in the regulation of inflammatory hyperalgesia was analyzed. Inflammatory hyperalgesia was induced by intraplantar injection of complete Freunds adjuvant (CFA) to the rat hind paw. NT-3 levels in the plantar skin were much higher than NGF levels (1.24 and 0.14 ng/g tissue, respectively) before CFA injection, but decreased significantly 6 h to 48 h after the injection while NGF was markedly induced at 6 h but decreased thereafter. When 1 microg of NT-3 was locally injected at 5 h after CFA injection at the time NT-3 levels decreased, hyperalgesia was reversed transiently but specifically. These results suggest an inhibitory role of NT-3 in the regulation of pain sensitivity.

Molecular cloning of cDNAs encoding α1, α2, and β subunits of rat brain platelet-activating factor acetylhydrolase1

Abstract Brain intracellular platelet-activating factor acetylhydrolase (PAF-AH(Ib)) is a tertiary G-protein-complex-like heterotrimeric enzyme which is composed of α1, α2, and β subunits and is implicated in stages of brain development such as the formation of the brain cortex. We have isolated and sequenced cDNA clones encoding these three subunits of rat brain PAF-AH(Ib). The amino acid sequences of brain PAF-AH has shown an extremely high homology among mammalian species. The tissue distribution of the three subunits was examined by Northern blot analysis. Although the mRNAs were detected in various organs, the ratio of the level of mRNA expression for the three subunits differed among rat tissues, raising the possibility that isoform(s) other than the heterotrimeric isoform exist in certain tissues.

Functional regulation of tactile sense by brain-derived neurotrophic factor in adult rats during acute inflammation

Nerve growth factor is present in skin in limiting amounts and is known to regulate the plasticity and the sensitivity of nociceptive neurons. Recently, knock-out mouse studies showed that neurotrophin-3 and brain-derived neurotrophic factor are required for the postnatal survival and functional maturation, respectively, of tactile sensory neurons. However, the roles of neurotrophin-3 and brain-derived neurotrophic factor in adult sensory neurons have not been clarified. Here, we report an unexpected and marked acute loss of tactile sense in the rat hind paw after adjuvant-induced inflammation. This loss was shown to be closely correlated with decreases in the expression of brain-derived neurotrophic factor, and to a lesser extent of neurotrophin-3 in the inflamed skin. Administration of brain-derived neurotrophic factor, but not neurotrophin-3, after inflammation accelerated the recovery of tactile sense. These results suggested a role of brain-derived neurotrophic factor in the physiological regulation of tactile sense in adulthood.

Enhancement or Suppression of ACE Inhibitory Activity by a Mixture of Tea and Foods for Specified Health Uses (FOSHU) That Are Marketed as "Support for Normal Blood Pressure"

The ACE inhibitory activities of mixtures of FOSHUs (Healthya, Goma-Mugicha, Lapis Support and Ameal) were examined in order to identify any antihypertensive interactions. Among combinations of Healthya with other samples that contain active peptides, only that with Ameal was found to have no inhibitory activity. Enhanced activity was observed in 2 other mixtures. The activity of a mixture of tea polyphenols and the whey component extracted from an Ameal solution was significantly decreased, thus demonstrating that whey protein lowered the ACE inhibitory activity of Healthya. Although oral administration of tea polyphenols alone significantly decreased SBP in SHR at 2 and 4 hr, combined administration with Ameal failed to decrease SBP at the same time points. In conclusion, the simultaneous intake of tea and FOSHUs that contain active peptides might affect daily self-antihypertensive management via enhancement or suppression of ACE inhibitory activity.