Acidic amino acid binding sites in mammalian neuronal membranes: their characteristics and relationship to synaptic receptors

Foster, Alan C.; Fagg, Graham E.

doi:10.1016/0165-0173(84)90020-1

Cited by 808 publications

(268 citation statements)

References 255 publications

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“…injected in a 5-fold higher concentration. Glutamate diethylester (GDEE), thought to be selective Oocytes injected with both the GluRl-specific and for quisqualate receptors [26], showed essentially no inthe GluR2-specific mRNA displayed larger current hibitory effect, but exhibited weak agonist activity. The responses to 30 PM L-glutamate, 100 ,uM kainate and 1 NMDA receptor antagonist D-(-)-2-amino-5-phos-,uM quisqualate than those injected with the GluRlphonovaleric acid (APV) slightly inhibited the'response specific mRNA alone ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Functional expression from cloned cDNAs of glutamate receptor species responsive to kainate and quisqualate

et al. 1990

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The complete amino acid sequences of two mouse glutamate receptor subunits (GluRl and GluR2) have been deduced by cloning and sequencing the cDNAs. Xenopus oocytes injected with mRNA derived from the GluRl cDNA exhibit current responses both to kainate and to quisqualate as well as to glutamate, whereas oocytes injected with mRNA derived from the GluR2 cDNA show little response. Injection of oocytes with both the mRNAs produces current responses larger than those induced by the GluRl-specific mRNA and the dose-response relations indicate a positively cooperative interaction between the two subunits. These results suggest that kainate and quisqualate can activate a common glutamate receptor subtype and that glutamate-gated ionic channels are hetero-oligomers of different subunits.

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Section: Resultsmentioning

confidence: 99%

Functional expression from cloned cDNAs of glutamate receptor species responsive to kainate and quisqualate

et al. 1990

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“…The role of NMDA receptors in the stimulation of neurite outgrowth by endogenous glutamate was examined by growing the cells in the presence of the selective NMDA receptor antagonist [3,4] D-2-amino-5-phosphonovalerate (APV). APV inhibited neurite outgrowth to the same extent as kynurenate ( fig.3) and the inhibition by APV was r _T_.…”

Section: Resultsmentioning

confidence: 99%

“…One possibility is that conventional neurotransmitters could regulate neuronal differentiation. Glutamate is a major excitatory neurotransmitter in the CNS which acts on three receptor types classified on the basis of their agonists as quisqualate, kainate or N-methyl-D-aspartate (NMDA) receptors [3,4]. Activation of NMDA but not the other two classes of glutamate receptors results in the opening of channels that allow Ca 2+ influx [5] and leads to a rise in cytosolic free Ca 2+ [6,7].…”

Section: Introductionmentioning

confidence: 99%

Glutamate acting on NMDA receptors stimulates neurite outgrowth from cerebellar granule cells

1987

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The effect of endogenous glutamate on neurite outgrowth from cerebellar granule cells in culture was examined. Neurite outgrowth was inhibited by enzymatic removal of endogenous glutamate from the culture medium. The broad-spectrum glutamate receptor antagonist kynurenate also inhibited neurite outgrowth from granule cells in serum-containing and serum-free cultures; the inhibition by kynurenate was reversed by exogenous glutamate. Neurite outgrowth was inhibited to the same extent by the NMDA receptor antagonist APV. These results indicate that endogenous glutamate, possibly released by granule cells themselves, stimulated neurite outgrowth through activation of the NMDA class of glutamate receptors. Activation of NMDA receptors on developing neurons may be an important mechanism for the regulation of neuronal growth and differentiation.

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“…The mechanisms by which excess exposure to glutamate can lead to this potentially important neuronal cell injury are not well understood and depend considerably on extrapolation from the better defined phenomenon of glutamate neuroexcitation. Several studies of the pharmacology of glutamate neuroexcitation have suggested that it is mediated by action on perhaps 3 subclasses of postsynaptic receptors, each named by a defining selective agonist: N-methyl-D-aspartate (NMDA), quisqualate (QUIS), and kainate (RAIN) (Watkins and Evans, 198 1;Foster and Fagg, 1984). The NMDA subclass is the best characterized, in part due to the availability of selective antagonists, such as m-2-amino-5-phosphonovalerate (APV) (Davies et al,198 1).…”

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confidence: 99%

Pharmacology of glutamate neurotoxicity in cortical cell culture: attenuation by NMDA antagonists

1988

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The antagonist pharmacology of glutamate neurotoxicity was quantitatively examined in murine cortical cell cultures. Addition of 1- 3 mM DL-2-amino-5-phosphonovalerate (APV), or its active isomer D-APV, acutely to the exposure solution selectively blocked the neuroexcitation and neuronal cell selectively blocked the neuroexcitation and neuronal cell loss produced by N-methyl-D-aspartate (NMDA), with relatively little effect on that produced by either kainate or quisqualate. As expected, this selective NMDA receptor blockade only partially reduced the neuroexcitation or acute neuronal swelling produced by the broad-spectrum agonist glutamate; surprisingly, however, this blockade was sufficient to reduce glutamate- induced neuronal cell loss markedly. Lower concentrations of APV or D- APV had much less protective effect, suggesting that the blockade of a large number of NMDA receptors was required to acutely antagonize glutamate neurotoxicity. This requirement may be caused by the amplification of small amounts of acute glutamate-induced injury by subsequent release of endogenous NMDA agonists from injured neurons, as the “late” addition of 10–1000 microM APV or D-APV (after termination of glutamate exposure) also reduced resultant neuronal damage. If APV or D-APV were present both during and after glutamate exposure, a summation dose-protection relationship was obtained, showing substantial protective efficacy at low micromolar antagonist concentrations. Screening of several other excitatory amino acid antagonists confirmed that the ability to antagonize glutamate neurotoxicity might correlate with ability to block NMDA-induced neuroexcitation: The reported NMDA antagonists ketamine and DL-2-amino- 7-phosphono-heptanoate, as well as the broad-spectrum antagonist kynurenate, were all found to attenuate glutamate neurotoxicity substantially; whereas gamma-D-glutamylaminomethyl sulfonate and L- glutamate diethyl ester, compounds reported to block predominantly quisqualate or kainate receptors, did not affect glutamate neurotoxicity. The present study suggests that glutamate neurotoxicity may be predominantly mediated by the activation of the NMDA subclass of glutamate receptors--occurring both directly, during exposure to exogenous compound, and indirectly, due to the subsequent release of endogenous NMDA agonists. Given other studies linking NMDA receptors to channels with unusually high calcium permeability, this suggestion is consistent with previous data showing that glutamate neurotoxicity depends heavily on extracellular calcium.

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Acidic amino acid binding sites in mammalian neuronal membranes: their characteristics and relationship to synaptic receptors

Cited by 808 publications

References 255 publications

Functional expression from cloned cDNAs of glutamate receptor species responsive to kainate and quisqualate

Functional expression from cloned cDNAs of glutamate receptor species responsive to kainate and quisqualate

Glutamate acting on NMDA receptors stimulates neurite outgrowth from cerebellar granule cells

Pharmacology of glutamate neurotoxicity in cortical cell culture: attenuation by NMDA antagonists

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