6B4 proteoglycan and a subset of GABAergic neurons in the cerebral cortex of adult rats

s141

THE EXPRESSION

235

PRIMARY

JUNK1 YAMAMOTO, NAM1 KAWAGUCHI Department

OF CXC AND CC CHEMOKINE

CULTURED

MICROGLIA,

ASTROCYTE

MASABUMI MINAMI, ATSUSHI and MASAMICHI SATOH

of Molecular

Pharmacology,

RECEPTOR mRNAs IN RAT

NISHIYORI,

Faculty of Pharmaceutical

AND NEURON. SHINYA TAKAMI,

Sciences,

YOSHIKAZU

Kyoto University,

Sakyo-ku,

OHTANI,

Kyoto 606-8501

CINC- 1, which is the member of CXC chernokine family, decreased the nocice-

Previously, we reported that intracerebroventricular

ptive threshold to mechanical stimuli and that the expression of the mRNAs for MCP-I and MIP-lc(, which are belonged to the CC chemokine family, were induced on glial cells after focal cerebral ischemia in the rat. However, the cellular sources of CXC and CC chemokine receptors (CXCRs and CCRs) are unknown. chemokine polymerase

receptors

In this study, we examined the expression of the mRNAs for CXC and CC

(CXCRs and CCRs) in rat primary cultured microglia, astrocytes

chain reaction (RT-PCR) technique.

subtypes of CCRs from rat brain.

and neuron by a reverse transcription

-

Firstly, we cloned the partial cDNAs for three subtypes of CXCRs and five

Next, we designed primer sets for each receptors based on the obtained partial cDNAs, and made

it possible to examine the expression of CXCR and CCR mRNAs by RT-PCR. The mRNAs for CXCR- I, 2.4 were expressed in rat primary cultured microglia, astrocytes and neuron.

While, the CCR mRNAs showed the various expression patterns in these cells.

These results suggest that the responses of the brain cells to the chemokines differ with cell types.

236

PERlNEURONAL

GLIAL PLEXUSES

PROTEOGLYCAN

AND A SUBSET OF GABAERGIC

CONTAINING

NEUROCANNEURONS

I?(, AND/OR PHOSPHACAN!hB4 IN THE CEREBRAL

CORTEX OF

ADULT RATS. MASAKONISHIZUKA’, ‘Departmentof

ATSUHIKO

Anatomy, Juntendo Umverslt> School of Medlclne, Bunkyo-ku,

‘Department of Perinatologq, Neurocan,

Its C-fragment

variant of receptor-type three antibodies, cell processes

Institute for Developmental

(neurocan-C)

and N-fragment

protein phosphatase

(neurtxan-130),

and phosphacan

and neurocan-130,

but not neurocan-C.

four types of penneuronal

GABAergic neruons immunoreactive

to anti-parlalbumm

an e\tracellular Using dtfferenr

in the c)-toplasm of ghal

Based on co-localization

of neurtran-

glial plexuses are distingulshed

containing glial plexuses; phosphacan-containing

we report, type of proteoglycan(s)

(tiB4 proteoglycan,

of neural proteoglycans.

plexuses; the remaining that are not clearly Immunoreactl\‘e

In this presentation,

237

Kasugal, Alchi 480-0303

(RF’TPP) are major components

m the cytoplasm of glial cell processes,

co-localized

Tok1.o I 13-842 1,

the cell bodies and proximal dendrites of a subset of neurons.

cerebral cortex of adult rats: neurocan-130 phosphacan

mPc

Research,

we have shown distribution of phosphacan

enwrapping

130 and phosphacan

antibodies.

OOHIRA ’

In the

plexuses; neurocan- I30 and

to the ant]-neurocan/phosphacan

contamed in the perineuronal

ghal pie\-uses of a subset of

antibocly In the cerebral cortex of adult rats.

KAINIC ACID-INDUCED ACTIVATION OF NUCLEAR FACTOR-KB IN THE GLIAL CELLS

YASUJI MATSUOKA ‘, MITSUHIRO OKAZAKI ‘, YOSHIHISA KITAMURA ‘, AND TAKASHI TANIGUCHI ’ ’ DEPARTMENT

OF NEUROBIOLOGY,

KYOTO PHARMACEUTICAL

UNIVERSITY, YAMASHINA,

KYOTO

607-8412 Nuclear factor-& (NF-KB) is known to play a key role in immune and inflammatory responses. It is known that inflammatory activation was occurred by neuronal damage. To understand the mechanisms of inflammatory activation which accompanies neuronal damage, we determined the cell type in which NF-KB was activated. NF-KB protein was detected in the cytosolic fraction in untreated and vehicle-treated rat hippocampus. After kainic acid (KA) treatment, NF-KB protein was significantly increased in both the cytosolic and particulate fractions. NF-KB-immunoreactivity was observed in both brain blood vessels and glial cells after 1 day. Although NF-KB-immunoreactivity in brain blood vessels disappeared after 3 days, this activity was maintained in glial cells for up to 7 days. In addition, double immunostaining indicate that NF-KB was activated in both glial cells such as microglia and astrocytes after 3 days. Thus, NF-KB activation seems to occur delayed and continuously in microglia and astrocytes, suggesting that an inflammatory activation in glial cells participates with KA-induced neurodegeneration.