The antagonistic action of glutamic acid diethylester towards amino acid-induced and synaptic excitations of central neurones

Haldeman, Scott; McLennan, H.

doi:10.1016/0006-8993(72)90470-2

Cited by 156 publications

(22 citation statements)

References 13 publications

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“…The finding of Haldeman & McLennan (1972) that glutamic acid diethylester blocks the excitatory action of iontophoretically applied glutamic acid and also synaptic activation of dorsal hom interneurones in the cat spinal cord and in the thalamus (Haldeman, Huffman, Marshall & McLennan, 1972) is an interesting development in this respect.…”

Section: Introductionmentioning

confidence: 99%

Alternative Approaches to Analgesia: Baclofen as a Model Compound

Cutting

Jordan

1975

British J Pharmacology

104

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Section: Introductionmentioning

confidence: 99%

Alternative Approaches to Analgesia: Baclofen as a Model Compound

Cutting

Jordan

1975

British J Pharmacology

104

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“…They exert potent excitatory action towards neuronal action potentials when applied iontophoretically (Curtis et al, 1972;Johnson, 1972) in nearly every part of the brain tested. Several antagonists to the action of glutamate have been suggested; glutamic acid diethyl ester (GDEE) among them has been reported to reduce the excitatory effects of glutamate without affecting responses to acetylcholine (ACh) in spinal cord, cuneate nucleus, ventrobasal thalamus, lateral geniculate and cerebral cortex (Curtis et al, 1972;Haldeman & McLennan, 1972). Furthermore, GDEE blocks excitatory action of input pathways to some of these structures when applied iontophoretically (Haldeman & McLennan, 1972) or parenterally (Stone, 1973).…”

Section: Introductionmentioning

confidence: 99%

“…Several antagonists to the action of glutamate have been suggested; glutamic acid diethyl ester (GDEE) among them has been reported to reduce the excitatory effects of glutamate without affecting responses to acetylcholine (ACh) in spinal cord, cuneate nucleus, ventrobasal thalamus, lateral geniculate and cerebral cortex (Curtis et al, 1972;Haldeman & McLennan, 1972). Furthermore, GDEE blocks excitatory action of input pathways to some of these structures when applied iontophoretically (Haldeman & McLennan, 1972) or parenterally (Stone, 1973). Glutamic acid dimethyl ester (GDME) is a glutamate uptake blocker (Haldeman & McLennan, 1973) and has been shown in various preparations to potentiate cellular responses to glutamate.…”

Section: Introductionmentioning

confidence: 99%

Glutamate Antagonists in Rat Hippocampus

Segal

1976

British J Pharmacology

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I Hippocampal cellular responses to acidic amino acids and some of their antagonists were measured in the rat anaesthetized with urethane. The effects of these antagonists on the field responses of the rat hippocampus to afferent stimulation were measured in acute as well as chronically prepared rats.2 Hippocampal pyramidal cells were excited by microiontophoretic application of glutamate and aspartate. These responses were antagonized by glutamic acid diethyl ester (GDEE), glutamic acid dimethyl ester (GDME) and by proline. Partial specificity could be seen as excitatory responses to acetylcholine were less susceptible to the antagonists. 3 Field responses of the hippocampus to commissural stimulation were reduced significantly in both an acutely prepared or the conscious rat following parenteral administration of GDEE and GDME but not proline. Responses to perforant path stimulation were not affected by these drugs. 4 It is suggested that an acidic amino acid may serve as a neurotransmitter in the commissural path to.area CAl of the dorsal hippocampus.

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“…Numerous early studies demonstrated that glutamate is the neurotransmitter of all these excitatory thalamic inputs (Haldeman and McLennan, 1972;de Biasi et al, 1994; reviewed by Salt and Eaton, 1996). Recent neuropharmacological findings have shown that the ascending excitatory afferents to both the ventral posterior and lateral geniculate nuclei (LGN) elicit responses in relay neurons that are sensitive to both non-N-methyl-D-aspartate (NMDA) and NMDA receptor antagonists.…”

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confidence: 99%

Subcellular distribution of AMPA and NMDA receptor subunit immunoreactivity in ventral posterior and reticular nuclei of rat and cat thalamus

Liu

1997

J. Comp. Neurol.

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Alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) selective glutamate receptors mediate excitatory neurotransmission in the somatosensory thalamus, but morphological localization of the receptors at identified thalamic synapses has been lacking. The authors used electron microscopic immunocytochemistry to localize AMPA selective GluR 2/3 subunits (GluR2/3) and NMDA receptor subunit 1 (NMDAR1) in rat and cat ventral posterior lateral nucleus (VPL) and in the associated sector of the reticular nucleus (RTN). Light microscopy showed that GluR2/3 and NMDAR1 immunolabeled neurons are homogeneously distributed in both nuclei. The relationship between glutamate receptor labeled profiles and glutamate or gamma-aminobutyric acid (GABA) labeled synapses was revealed by combining preembedding and postembedding immunostaining at the electron microscopic level. GluR2/3 and NMDAR1 immunoreactivity was located in somata and in proximal and distal dendrites of VPL relay cells and of RTN cells. Immunoreactivity was concentrated in postsynaptic densities of glutamatergic synapses and absent from postsynaptic densities of GABAergic synapses. In the cat, GluR2/3 and NMDAR1 immunoreactivity was also localized in GABAergic interneurons, including their presynaptic dendrites (PSD). Of the GluR2/3 and NMDAR1 labeled thalamic synapses observed, 10-29% were lemniscal (RL) type synapses in VPL; 60-70% were corticothalamic (RS) type synapses in the VPL and RTN. In the cat, 7-19% were identified as PSD profiles, and more NMDAR1 labeled PSD were found in the VPL than in the RTN. The main findings were as follows: 1) AMPA selective GluR2/3 and NMDAR1 share similar distribution patterns in the rat and cat somatosensory thalamus, 2) both glutamate receptors are likely to be colocalized at postsynaptic densities of both RL and RS synapses, and 3) localization of the glutamate receptor proteins in GABAergic dendrites in the cat thalamus indicates that glutamatergic transmission to GABAergic neurons is also mediated by both NMDA and non-NMDA receptors.

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The antagonistic action of glutamic acid diethylester towards amino acid-induced and synaptic excitations of central neurones

Cited by 156 publications

References 13 publications

Alternative Approaches to Analgesia: Baclofen as a Model Compound

Alternative Approaches to Analgesia: Baclofen as a Model Compound

Glutamate Antagonists in Rat Hippocampus

Subcellular distribution of AMPA and NMDA receptor subunit immunoreactivity in ventral posterior and reticular nuclei of rat and cat thalamus

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