c-kit on mossy fiber-CA3 synaptic potentiation in mice

S146

ROLES OFSTEM

245

CELL FACTOR/C-KIT

TETSUYA

KONDO. TOSHIHIKO

KATAFUCHI

Dcpartmcnt

of PhysioloRy,Kvush~1

University

TAKESHI

ON MOSSY FIBER-CA3

SYNAPTIC

POTENTIATION

AND TETSURO Faculty

FUJII, KAZUO Z. SATO, YOSHIHIRO

Department of Pharmacology, We have demonstrated

of Mcdicinc,Fukuoka

WATANABE,

Kyoritsu College of Pharmacy,

that acetylcholine

HORI 812.8582Japan

MARIKA MATSUI, KOICHIRO

Minato-ku,

(ACh), a classical neurotransmitter,

various muscarinic (MS) ACh receptors has been reported in lymphocytes. in regulation of interactions between the nervous and immune systems. ACh in regulation of the immune systems,

KAWASHIMA

Tokyo 105-8512 is present in the blood of different species of

mammals including humans, and that blood ACh mainly originates from T-lymphocytes.

In addition, mRNA expression

These findings suggest involvement

In this study, we investigated the physiological

by analyzing the effect of bethanechol

induced a rapid and transient increase of intraceUular calcium ion concentration of [C%+]i (calcium oscillation) was observed with time in CEM. However,

([caZ+]i).

ATSUSHI

TAKAKI1.2,

calcium oscillation via MS ACh receptor

[Dept. of Physiology, Tokyo 142-8555

SEIJI YAGII,

a Ca channel Ca channels.

STRESS IN RAT

and’rETSUR0

Kyushu Univ. Fat. of Med., Fukuoka 812-8582, 2Dept. of Anatomy,

Plasma interleukin-6 stress.

AXIS DURING NON-INFLAMMATORY

SEIJI SHIODA2, YOSHIO KANEMITSLJI,

BeCh

In addition, an intermittent increase

These results indicate that calcium oscillation may be maintained via Ca2+ entry from receptor-operated

BRAIN-GUT-LIVER-IMMUNE

role of

(BeCh), a selective MS ACh receptor

stimulation was not observed in the absence of external Ca2+, or abolished in the presence of 1 FM nicardipine,

247

for

of blood ACh

agonist, on intracelIular calcium signals in CEM, a human leukemic T-cell line, used as a model of lymphocytes.

blocker.

IN

MICE

HORIl

Showa Univ. School of Med.,

(IL-6) levels increase not only with infection and tissue damage but also with non-inflammatory

.

Our previous and current studies have suggested that the liver is one of the major sources of the increased IL-6 during

immobilization

stress

in the rat.

The hepatic

induction

of

IL-6 is thought

lipopolysaccharide

(LPS) based on the following

findings:

viva neutralization

of LPS. 2) The concentration

of LPS in the hepatoportal

(FITC)-labeled

1) Immobilization

to be mediated

by enteric

( IM ) -induced IL-6 increase is abolished by in vein increases during IM. 3) A fluorescent

LPS injected into the intestinal lumen was detected in Kupffer cells and sinusoidal endothelial

78 % of which are also stained with an anti-IL-6 antibody. activated during non-inflammatory

flora-derived

cells after IM,

All these results suggest that the Brain-Gut-Liver-Immune

stress, and that the gut-derived

LPS plays a critical role in this mechanism.

dye

axis is