Stereoselective antagonism of NMDA-stimulated noradrenaline release from rat hippocampal slices by MK-801

Lalies, Margaret D.; Middlemiss, Derek N.; Ransom, Richard W.

doi:10.1016/0304-3940(88)90703-3

Cited by 31 publications

(12 citation statements)

References 11 publications

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“…These observations confirm that NMDA-and KA-evoked neurotransmitter release is mediated by actions at distinct EAA-receptor subtypes. These conclusions are similar to those of previous investigations on hippocampal brain slices (Lehman & Scatton, 1982;Jones et al, 1987;Schmidt & Taylor, 1988;Lalies et al, 1988). The results of the present investigation suggest that the EAA-receptors mediating the evoked release of [3H]-noradrenaline are similar in both cortical and hippocampal tissues.…”

Section: Discussionsupporting

confidence: 93%

Inhibition of N‐methyl‐D‐aspartate‐ and kainic acid‐induced neurotransmitter release by ω‐conotoxin GVIA

Keith

Mangano

Salama

1989

British J Pharmacology

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Section: Discussionsupporting

confidence: 93%

Inhibition of N‐methyl‐D‐aspartate‐ and kainic acid‐induced neurotransmitter release by ω‐conotoxin GVIA

Keith

Mangano

Salama

1989

British J Pharmacology

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“…In the present study, evidence is presented that NMDA receptors are, in fact, involved in the release of [3H]GABA from cortical GABAergic interneurons. This conclusion can be drawn from the ability of the competitive NMDA receptor antagonist CGP 37849 (Fagg et al, 1989;Fink et al, 1992) and ofdizocilpine [which blocks the NMDA-gated ion channel by interacting with the phencyclidine site within this channel (Lalies et al, 1988;Lodge and Johnson, 1990)] to counteract the NMDA-evoked [3H]GABA release. A stimulant effect of NMDA receptor activation on NA release in the cerebral cortex has already been established under the present conditions in rat (Fink et al, 1989) and human (Fink et al, 1992) cortical slices.…”

Section: Discussionmentioning

confidence: 99%

Increased GABA Release in the Human Brain Cortex as a Potential Pathogenetic Basis of Hyperosmolar Diabetic Coma

Fink

Zentner

Göhert

1994

Journal of Neurochemistry

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Human cerebral cortical slices preincubated with [3H]GABA, [3H]noradrenaline, or 5-[3H]hydroxytryptamine and superfused with Krebs solution or Mg2+free Krebs solution were used to investigate the influence of increased D-glucose concentrations on the release of these [3H]-neurotransmitters evoked by high K+ content or NMDA receptor activation, respectively. An increase in level of D-glucose (normal content, 11.1 mM) by 32, 60, and/or 100 mM (a range characteristic for hyperosmolar diabetic coma) increased the [3H]GABA release and inhibited the [3H]noradrenaline release evoked by both methods of stimulation. The K+-induced 5-[3H]hydroxytryptamine release was also inhibited by high D-glucose content. Blockade of GABA, receptors by p-(3-aminopropyl)-p-diethoxymethylphosphinic acid (CGP 35348) attenuated the inhibitory effect of high D-glucose content on the K+-evoked release of [3H]noradrenaline and 5-[3H]hydroxytryptamine, suggesting that the effect on monoamine release is, at least to a major part, the result of the increased GABA release and, as a consequence, of an increased GABA concentration at inhibitory GABA, receptors. The membrane-impermeable sorbitol mimicked the increasing effect of D-glucose on [3H]GABA release and its inhibitory effect on 5-[3H]hydroxytryptamine release. However, dimethyl sulfoxide, which is known to permeate rapidly through biological membranes, had no effect at concentrations equiosmolar to D-glucose. It is concluded that a reduction in brain cell volume caused by increased extracellular, compared with cytoplasmic, osmolarity is crucial for the changes in neuronal function observed at high Dglucose and sorbitol content. In view of the fact that GABA is the main inhibitory neurotransmitter in the brain, the increased GABA release may be assumed to contribute to the pathogenesis of hyperosmolar diabetic coma.

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“…To determine whether glutamate-evoked adenosine release was mediated through NMDA receptors, the effects of the competitive NMDA receptor antagonist, APV (1 mM), and the noncompetitive NMDA receptor antagonist, MK-80 1 (3 pM), on glutamate-evoked adenosine release were determined. At these concentrations, both compounds have been shown to effectively block the NMDA receptor-mediated release of various neurotransmitters from rat brain slices (Lehmann and Scatton, 1982;Snell and Johnson, 1986;Lalies et al, 1988). Neither APV nor MK-80 1 affected basal adenosine release (not shown).…”

Section: Involvement Of Nmda and Non-nmda Receptors In Glutamate-evokmentioning

confidence: 91%

Role of Excitatory Amino Acid Receptors in K⁺‐and Glutamate‐Evoked Release of Endogenous Adenosine from Rat Cortical Slices

Hoehn

White

1990

Journal of Neurochemistry

104

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K+ and glutamate released endogenous adenosine from superfused slices of rat parietal cortex. The absence of Ca2+ markedly diminished K+- but not glutamate-evoked adenosine release. Tetrodotoxin decreased K+- and glutamate-evoked adenosine release by 40 and 20%, respectively, indicating that release was mediated in part by propagated action potentials in the slices. Inhibition of ecto-5'-nucleotidase by alpha,beta-methylene ADP and GMP decreased basal release of adenosine by 40%, indicating that part of the adenosine was derived from the extracellular metabolism of released nucleotide. In contrast, inhibition of ecto-5'-nucleotidase did not affect release evoked by K+ or glutamate, suggesting that adenosine was released as such. Inhibition of glutamate uptake by dihydrokainate potentiated glutamate-evoked release of adenosine. Glutamate-evoked adenosine release was diminished 50 and 55% by the N-methyl-D-aspartate (NMDA) receptor antagonists, DL-2-amino-5-phosphonovaleric acid and (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801), respectively. The remaining release in the presence of MK-801 was diminished a further 66% by the non-NMDA receptor antagonist, 6,7-dinitroquinoxaline-2,3-dione, suggesting that both NMDA and non-NMDA receptors were involved in glutamate-evoked adenosine release. Surprisingly, K+-evoked adenosine release was also diminished about 30% by NMDA antagonists, suggesting that K+-evoked adenosine release may be partly mediated indirectly through the release of an excitatory amino acid acting at NMDA receptors.

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Stereoselective antagonism of NMDA-stimulated noradrenaline release from rat hippocampal slices by MK-801

Cited by 31 publications

References 11 publications

Inhibition of N‐methyl‐D‐aspartate‐ and kainic acid‐induced neurotransmitter release by ω‐conotoxin GVIA

Inhibition of N‐methyl‐D‐aspartate‐ and kainic acid‐induced neurotransmitter release by ω‐conotoxin GVIA

Increased GABA Release in the Human Brain Cortex as a Potential Pathogenetic Basis of Hyperosmolar Diabetic Coma

Role of Excitatory Amino Acid Receptors in K⁺‐and Glutamate‐Evoked Release of Endogenous Adenosine from Rat Cortical Slices

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Stereoselective antagonism of NMDA-stimulated noradrenaline release from rat hippocampal slices by MK-801

Cited by 31 publications

References 11 publications

Inhibition of N‐methyl‐D‐aspartate‐ and kainic acid‐induced neurotransmitter release by ω‐conotoxin GVIA

Inhibition of N‐methyl‐D‐aspartate‐ and kainic acid‐induced neurotransmitter release by ω‐conotoxin GVIA

Increased GABA Release in the Human Brain Cortex as a Potential Pathogenetic Basis of Hyperosmolar Diabetic Coma

Role of Excitatory Amino Acid Receptors in K+‐and Glutamate‐Evoked Release of Endogenous Adenosine from Rat Cortical Slices

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Role of Excitatory Amino Acid Receptors in K⁺‐and Glutamate‐Evoked Release of Endogenous Adenosine from Rat Cortical Slices