Kainic acid stimulates excitatory amino acid neurotransmitter release at presynaptic receptors

Ferkany, John W.; Zaczek, Robert; Coyle, Joseph T.

doi:10.1038/298757a0

Cited by 279 publications

(103 citation statements)

References 21 publications

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“…In our laboratory slight effects of N-methyl D-aspartate (NMDA) and quisqualate on glutamate release, which have also been reported by Sherman et al (1992), did not respond to established antagonists of NMDA and 2-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors (McMahon et al, 1989). Presynaptic effects of kainate (Ferkany and Coyle, 1982) can be accounted for by its ability to inhibit the acidic amino acid transporter , although a G-proteincoupled action of kainate has also been proposed (Brammer et al, 1991).…”

Section: The Acute Regulation Of Glutamate Exocytosismentioning

confidence: 94%

The glutamatergic nerve terminal

Nicholls

1993

European Journal of Biochemistry

208

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Glutamate as a neurotransmitterThe human brain has about lolo neurones, each of which, on average, makes about 1000 synaptic contacts with other neurones. Of these l O I 3 synapses perhaps up to 90% utilize amino acids as their neurotransmitter. Glutamate is the major excitatory amino acid (acting predominantly on depolarizing post-synaptic receptors) while 4-aminobutyrate (GABA) and glycine are the major inhibitory transmitters (acting on hyper-polarizing receptors). As well as playing the dominant role in fast information transfer, glutamate is of particular interest in view of its involvement in current models of memory and learning (Bliss and Dolphin, 1982;Cotman et al., 1988;Collingridge and Singer, 1990) and because a pathological release of glutamate in brain ischaemia is neurotoxic and a major contributor to the damage caused under these conditions (Rothman and Olney, 1986;Choi, 1988 ;Meldrum and Garthwaite, 1990).A synapse has a pre-synaptic element responsible for the storage and release of transmitter and a post-synaptic element containing one or more classes of receptor for the transmitter. The potent combination of electrophysiology and molecular cloning has allowed a dramatic advance in our understanding of post-synaptic events. Three classes of post-synaptic ionotropic (possessing an integral ion channel) glutamate receptors have been identified and cloned: the 2-amino-3-hydroxy-5-methyl-4-isoxazole propionatekainate (AMPA/ KA) receptor Nakanishi et al., 1990;Sakmann, 1992), the high-affinity KA receptor (Egebjerg et al., 1991) and the N-methyl D-aSpartate (NMDA) receptor (Moriyoshi et al., 1991 ; Kumar et al., 1991 ;Barnard, 1992). Each can exist in many isoforms by combining subunits formed from distinct genes, by alternative splicing or by post-transcriptional modification (Monyer et al., 1991 ;Burnashev et al., 1992).The AMPNKA receptor is responsible for fast information transfer while the NMDA receptor is only operative when the post-synaptic membrane is independently depolarized by another receptor. This 'associative' behaviour of the latter is believed to underlie aspects of the learning process.

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Section: The Acute Regulation Of Glutamate Exocytosismentioning

confidence: 94%

The glutamatergic nerve terminal

Nicholls

1993

European Journal of Biochemistry

208

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“…The central effect of kainate appears to propagate through an increase in the release of glutamate and aspartate after activation of presynaptic kainate receptors, depolarization after activation of postsynaptic a-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainate receptors, and the secondary activation of N-methyl-d-aspartate (NMDA) receptors. 12,24 In support of this, NMDA antagonists as well as AMPA/kainate antagonists were reported to attenuate kainate-induced neuronal death and seizure activity. 6,8,9,11,22 Several studies suggest that kainate neurotoxicity may be mediated through down-regulation of glutamate receptor subunit 2 expression in the degenerating hippocampal areas, 14,32 which is expected to enhance Ca 2ϩ permeability through non-NMDA receptors and trigger neuronal death.…”

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confidence: 85%

Nuclear factor kappa B-mediated kainate neurotoxicity in the rat and hamster hippocampus

Won

Kim

et al. 1999

Neuroscience

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“…L-[G-3H]Glutamic acid of specific radioactivity of [29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45] Ci/mmol (1 Ci = 37 GBq) was purchased from Amersham. Triton X-100 (gas chromatographic grade) and the L and D isomers of glutamic and aspartic acids were obtained from Merck; NMeAsp, quinolinic, and kainic acids, from Sigma; quisqualic, ibotenic, DL-2-amino-5-phosphonovaleric (DL-APV), and DL-2-amino-7-phosphonoheptanoic (DL-APH) acids, from Cambridge Research Biochemicals (Harston, U.K.); and DL-2-amino-3-phosphonopropionic acid and DL-APB, from Calbiochem (La Jolla, CA).…”

mentioning

confidence: 99%

Selective association of N-methyl aspartate and quisqualate types of L-glutamate receptor with brain postsynaptic densities.

Fagg¹,

Matus²

1984

Proc. Natl. Acad. Sci. U.S.A.

182

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Recognition sites for the excitatory neurotransmitter, L-glutamate, were studied in synaptic plasma membranes and postsynaptic densities (PSDs) isolated from rat brains. The results demonstrate (i) that L-glutamate binding sites may be resolved into three distinct subtypes (categories Al, A2, and A4), each corresponding to an electrophysiologically identified receptor class, and (it) that the N-methyl aspartate (Al) ), which is the major population present in SPMs, is absent from the PSD. Those sites present in PSDs may be subdivided into two populations which, as in the case of the electrophysiologically derived receptor classification scheme, are differentially sensitive to N-methyl DL-aspartate (NMeAsp) and quisqualate (sites Al and A2, respectively).MATERIALS AND METHODS Chemicals. L-[G-3H]Glutamic acid of specific radioactivity of 29-45 Ci/mmol (1 Ci = 37 GBq) was purchased from Amersham. Triton X-100 (gas chromatographic grade) and the L and D isomers of glutamic and aspartic acids were obtained from Merck; NMeAsp, quinolinic, and kainic acids, from Sigma; quisqualic, ibotenic, DL-2-amino-5-phosphonovaleric (DL-APV), and DL-2-amino-7-phosphonoheptanoic (DL-APH) acids, from Cambridge Research Biochemicals (Harston, U.K.); and DL-2-amino-3-phosphonopropionic acid and DL-APB, from Calbiochem (La Jolla, CA). DL-2-amino-6-phosphonohexanoic acid was kindly provided by J. F. Collins (London). Subcellular Fractionation. SPMs and PSDs were isolated from fresh brains (excluding brainstem) of adult male rats (strain RAI, 180-250 g; Ciba-Geigy). The SPM fraction was prepared by the method of Jones and Matus (19), and this was treated with either 0.5% or 1.0% Triton X-100, followed by centrifugation through 1.0 M sucrose, to yield PSDs (18,20) (the results obtained with either concentration of Triton X-100 were indistinguishable and were pooled). Fractions were washed four times by resuspension and cenAbbreviations: PSD, postsynaptic density; SPM, synaptic plasma membrane; APB, 2-amino-4-phosphonobutyrate; APH, 2-amino-7-phosphonoheptanoate; APV, 2-amino-5-phosphonovalerate; NMeAsp, N-methyl DL-aspartate; NMeDAsp, N-methyl D-aspartate. 6876The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "adiertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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Kainic acid stimulates excitatory amino acid neurotransmitter release at presynaptic receptors

Cited by 279 publications

References 21 publications

The glutamatergic nerve terminal

The glutamatergic nerve terminal

Nuclear factor kappa B-mediated kainate neurotoxicity in the rat and hamster hippocampus

Selective association of N-methyl aspartate and quisqualate types of L-glutamate receptor with brain postsynaptic densities.

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