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Your search keyword '"Chikuma, Toshiyuki"' showing total 81 results
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81 results on '"Chikuma, Toshiyuki"'

63. Interleukin-6 Induces Prostaglandin E2 Synthesis in Mouse Astrocytes.

Author

Chikuma, Toshiyuki, Yoshimoto, Tetsuya, Ohba, Masahiro, Sawada, Makoto, Kato, Takeshi, Sakamoto, Tomoaki, Hiyama, Yukio, and Hojo, Hiroshi

Abstract

The physiological function of interleukin-6 within the central nervous system (CNS) is complex; interleukin-6 exerts neurotrophic and neuroprotective effects and yet can also function as a mediator of inflammation, demyelination, and astrogliosis depending on the cellular context. However, the roles of interleukin-6 in astrocytes are poorly understood. In the present study, we investigated the effect of the pro-inflammatory cytokine interleukin-6 on the production of the inflammatory mediator prostaglandin E2 in mouse astrocytes. Interleukin-6 stimulated prostaglandin E2 production in a time-dependent fashion via a rapid and transient induction of cyclooxygenase-2 messneger RNA, followed by cyclooxygenase-2 protein synthesis. Interleukin-6 may act on the nervous system by interacting with its specific soluble interleukin-6 receptor and the signal transducer 130-kDa glycoprotein. Simultaneous treatment of astrocytes with interleukin-6 and soluble interleukin-6 receptor caused marked induction of prostaglandin E2 synthesis, and this effect was suppressed by adding a neutralizing antibody against soluble interleukin-6 receptor. Furthermore, the mouse 130-kDa glycoprotein antibody suppressed prostaglandin E2 formation induced by interleukin-6, as well as interleukin-6/soluble interleukin-6 receptor complexes, in a dose-dependent manner. These results indicate that interleukin-6/soluble interleukin-6 receptor complexes and the signal transducer 130-kDa glycoprotein play an important role in the regulation of cyclooxygenase-2 expression and subsequent prostaglandin E2 formation in mouse astrocytes and that interleukin-6 is an important regulator of immune and inflammatory processes in the CNS. [ABSTRACT FROM AUTHOR]

Published
2009
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70. The Effects of Morphine-Induced Increases in Extracellular Acetylcholine Levels in the Rostral Ventrolateral Medulla of Rat

Author

Taguchi, Kyoji, Kato, Masatoshi, Kikuta, Jun, Abe, Kenji, Chikuma, Toshiyuki, Utsunomiya, Iku, and Miyatake, Tadashi

Abstract

The present study examined the role of the rostral ventrolateral medulla (RVLM) in the modulation of acetylcholine (ACh) release by morphine. We examined the effect of morphine on the release of ACh in the RVLM of freely moving rats using the in vivo microdialysis method. The basal level of ACh was 303.0 ± 28.2 fmol/20 μl/15 min in the presence of neostigmine (10 μM). Morphine at a low dose of 5 mg/kg (i.p.) increased ACh release by the RVLM by 42.4%. A higher morphine dose (10 mg/kg i.p.) significantly increased the release of ACh by 75.4%, with a maximal effect (86.4%) at 75 min. This enhancement following i.p. administration of morphine was reversed by naloxone (1 mg/kg i.p.). Addition of morphine (10−4M) to the perfusion medium increased the ACh release by 85.8% of the predrug values. The increased ACh release induced by local application of morphine was reversed by pretreatment with naloxone (1 mg/kg i.p.). The antinociceptive effect of locally applied morphine into the RVLM was assessed using the hot-plate test and tail immersion test in unanesthetized rats. Local application of morphine (10−4M) via a microdialysis probe induced an increase in both tail withdrawal and hot-plate response. These findings suggest that morphine seems to exert a direct stimulatory effect on ACh release by the RVLM and that morphine-induced nociception is, in part, activated by the release of ACh in freely moving rats.

Published
1999
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