Patch-clamp analysis of glutamatergic synaptic transmission in thin slices of the basal ganglia

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PATCH-CLAMP ANALYSIS OF GLUTAMATERGIC SYNAPTIC TRANSMISSION IN THIN SLICES OF TIE BASAL GANGLIA. AKIHISA MORI. TETSUO TAKAHASHI*, YASUSHI MIYASHITA AND HARUO KASAI, Department of Phvsiologv, Facultv of Medicine, University of Tokvo, Honrro, Bunkvo-ku, Tokyo 113, Japan. Tight-seal whole-cell clamp experiments were performed on thin slices (150-250 p) obtained from the caudate nucleus of rats (9-14 days old). Most of the small cells (lo-15 w in diameter) stained with Lucifer Yellow exhibited long dendrites stubbed with fine spines, which is characteristic of medium-sized spiny neurons. Focal stimulation of the caudate nucleus with a glass pipette purely evoked excitatory synaptic currents in the presence of picrotoxin. The EPSCs were composed of NMDA and non-NMDA components; APV abolished the former component and CNQX the latter. Spontaneous EPSCs also comprised the two components, suggesting co-localization of the two receptor subtypes in the postsynaptic membranes. One feature of the ghttamatergic synaptic transmission was that, in the paired-pulsed experiments, the second EPSC was inhibited to 30% of the first EPSCs. This marked paired-pulse inhibition occurred both in the NMDA and non-NMDA components, showed no delay in onset and persisted up to 500 ms in the NMDA components, but only to 30 ms in the non-NMDA component. Quantal analysis suggested the involvement of a presynaptic mechanism in the inhibition of the non-NMDA component.

EXCITATORY

AMINO ACIDS

RELEASE

FROM CULTURED

HIPPOCAMPAL

CORD ASTROCYTES

AND SPINAL

INDUCED BY A HYPOXIC/HYPOGLYCEMIC TREATMENT YOICHI NAKAMURAl. TADANORI OGATA1*'.KIYOSHI KATAOKAI. Depts.of Physiology1and Orthopaedic Surgerv2. Ehime University, School of Medicine.Shigenobu,Ehime 791-02,Japan A postischemicbrain damage is caused by an elevationof extracellular concentrations of excitatory amino acids (EAA).

We demonstrate that the cultured astrocytesfrom hippocampus and

spinalcord releaseEAA by a hypoxic/hypoglycemic(ischemic)treatment. The amount of released EAA from the astrocyteswas much astrocytes

released

larger

than

that

from

the

cultured

neurons.

Interestingly,

more aspartate (Asp) than glutamate (Glu).although the endogenous

much

contentof Asp was lessthan Glu. By the ischemictreatment,the endogenous contentsof EAA in astrocyteswere not decreased but rather increased,while a large amount of the EAA was reThese resultssuggest that the ischemicneuronal death is due, at leastin part,to the

leased.

excitotoxicity of Asp derived from surrounding astrocytes.

EVIDENCE THAT GLUTAMATE-IHMUNOREACTIVENEURONS OF THE MEDIAL DIVISION NUCLEUS PROJECT

MITSUHIKO MIURA. Department 3-39-22

Showa-machi.

Glutamate

of

Physiology

Maebashi_shi.

immunoreactivity

using

ipsilaterally

a double-labeling

was

indicate

that

vasomotor No significant WKY rats.

to

the

technique

found the

are difference

present, was

Division,

371,

in 9X,

medial

in

neurons suggesting found

between

the

nucleus

in combination

with located

involvement the

Gunma

University

School

of

Medicine,

JaDan.

division

subretrofacial

possibly-glutamatergic

neurons

Ist

Gunma-ken

SHR rats, of neurons located in projecting

OF THE CENTRAL AHYGDALOID

TO THE SUBRETROFACI AL NUCLEUS OF SHR AND WKY RATS KI YOSHIGE TAKAYAHA. AND

case of

of WKY rats, the

(SRF) in the glutamate in of

distribution

the the

and

central

14X,

amygdaloid rostra1

in

CeM project

of

to

blood

labeled

case

of

(CeM)

ventrolateral

immunocytochemistry.

CeM in

the

nucleus

medulla The results

the

SRF,

pressure

CeM neurons

in

which

regulation. in

SHR and