Quisqualate, kainate and NMDA can initiate spreading depression in the turtle cerebellum
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Quisqualate, kainate and NMDA can initiate spreading depression in the turtle cerebellum. / Lauritzen, Martin; Rice, Margaret E.; Okada, Yoshio; Nicholson, Charles.
In: Brain Research, Vol. 475, No. 2, 20.12.1988, p. 317-327.Research output: Contribution to journal › Journal article › Research › peer-review
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T1 - Quisqualate, kainate and NMDA can initiate spreading depression in the turtle cerebellum
AU - Lauritzen, Martin
AU - Rice, Margaret E.
AU - Okada, Yoshio
AU - Nicholson, Charles
PY - 1988/12/20
Y1 - 1988/12/20
N2 - This study evaluated the role of excitatory amino acid (EAA) receptor activation in spreading depression (SD), using the in vitro turtle cerebellum as a model system. SD was triggered by electrical stimulation or by elevated K+ after the cerebellum had been conditioned for at least 30 min with physiological saline in which most of the chloride had been replaced by propionate. SD was recognized as a transient (1-3 min) negative shift of extracellular potential accompanied by depression of evoked potentials (15-30 min) and an increase of extracellular K+ up to 60 mM, which spread across the cerebellum at rates of 1-7 mm/min. SD usually commenced in the granular layer, which apparently contains the 3 major EAA receptor subtypes, quisqualate, kainate and N-methyl-d-aspartate (NMDA), then subsequently spread to the molecular layer, which is largely free of NMDA receptors. Glutamate, aspartate, NMDA, kainate and quisqualate all triggered SD. Kynurenic acid and 2-aminophosphonovaleric acid (APV) inhibited SD under certain conditions further suggesting involvement of EAA receptors. The initiation of SD was blocked by high Mg2+ and facilitated in low extracellular Mg2+, which also eliminated the delay in molecular layer SD onset. Our data suggest that no one EAA receptor subtype is singly responsible for SD.
AB - This study evaluated the role of excitatory amino acid (EAA) receptor activation in spreading depression (SD), using the in vitro turtle cerebellum as a model system. SD was triggered by electrical stimulation or by elevated K+ after the cerebellum had been conditioned for at least 30 min with physiological saline in which most of the chloride had been replaced by propionate. SD was recognized as a transient (1-3 min) negative shift of extracellular potential accompanied by depression of evoked potentials (15-30 min) and an increase of extracellular K+ up to 60 mM, which spread across the cerebellum at rates of 1-7 mm/min. SD usually commenced in the granular layer, which apparently contains the 3 major EAA receptor subtypes, quisqualate, kainate and N-methyl-d-aspartate (NMDA), then subsequently spread to the molecular layer, which is largely free of NMDA receptors. Glutamate, aspartate, NMDA, kainate and quisqualate all triggered SD. Kynurenic acid and 2-aminophosphonovaleric acid (APV) inhibited SD under certain conditions further suggesting involvement of EAA receptors. The initiation of SD was blocked by high Mg2+ and facilitated in low extracellular Mg2+, which also eliminated the delay in molecular layer SD onset. Our data suggest that no one EAA receptor subtype is singly responsible for SD.
KW - Aspartate
KW - Glutamate
KW - Ion-selective microelectrode
KW - Kainate
KW - N-methyl-d-aspartate
KW - Quisqualate
KW - Spreading depression
KW - Turtle cerebellum
UR - http://www.scopus.com/inward/record.url?scp=0024206707&partnerID=8YFLogxK
U2 - 10.1016/0006-8993(88)90620-8
DO - 10.1016/0006-8993(88)90620-8
M3 - Journal article
C2 - 2905624
AN - SCOPUS:0024206707
VL - 475
SP - 317
EP - 327
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 2
ER -
ID: 201456673