Factors affecting the release of purines from mouse cerebral cortex: Potassium removal and metabolic inhibitors

Lloyd, H.G.E.; Stone, T.W.

doi:10.1016/0006-2952(81)90304-x

Cited by 9 publications

(1 citation statement)

References 14 publications

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“…The results with verapamil are not conclusive in that although there was a consistent reduction in release due to KCl and NMDLA with this calcium antagonist the difference did not reach significant levels: This could represent either a failure to block completely all calcium movements with topically applied verapamil in vivo (this may be due to access difficulties) or that the release of labelled adenosine derivatives is not entirely calciumdependent. As previous studies with cortical slices showed a substantial reduction in release of labelled adenosine or its derivatives (Lloyd & Stone, 1981) with verapamil, this suggests the former explanation is more likely. In addition, Jhamandas & Dumbrille (1980) showed calcium-dependency of glutamateevoked release only when calcium-free medium and the addition of EGTA was employed, presumably reflecting the difficulty of depleting calcium in an in vivo system.…”

Section: Discunionsupporting

confidence: 63%

In vivo release of [³H]‐purines by quinolinic acid and related compounds

Perkins

Stone

1983

British J Pharmacology

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In vivo release of [3H]-purines from the cortex of anaesthetized rats was measured and the actions of excitatory amino acids and analogues investigated. 2 High KCl, N-methyl-DL-aspartate (NMDLA) and quinolinic acid produced a large increase in basal release of labelled materials. Glutamate, quisqualate and kainate had less effect. 3 The N-methyl-D-aspartic acid (NMDA)-preferring receptor antagonist, 2-amino-7-phosphonoheptanoic acid, significantly reduced the release evoked by NMDLA and quinolinate but not that produced by the other agonists. 4 Kynurenic acid, a compound metabolically related to quinolinic acid, reduced the release due to NMDLA and quinolinate but not glutamate. 5 The results add further support to the suggestion that quinolinic acid acts on the NMDApreferring receptor.

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Section: Discunionsupporting

confidence: 63%

In vivo release of [³H]‐purines by quinolinic acid and related compounds

Perkins

Stone

1983

British J Pharmacology

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Adenosine Release

Stone¹,

Newby²,

Lloyd³

1990

Adenosine and Adenosine Receptors

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Release and actions of adenosine in the central nervous system

et al. 1994

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Adenosine is released from active neurons into the extracellular fluid at a concentration of about 1 mumol/l. Neither the precise cellular origin nor the biochemical form of release has been firmly established, though the nucleotide is probably released partly directly, as a result of raised intracellular levels, and partly as nucleotides, which are subsequently hydrolysed. Once in the extracellular medium, adenosine markedly inhibits the release of excitatory neurotransmitters and modulatory peptides and has direct inhibitory effects on postsynaptic excitability via A1 receptors. A population of A2 receptors may mediate depolarization and enhanced transmitter release. Adenosine also modulates neuronal sensitivity to acetylcholine and catecholamines, all these effects probably contributing to the behavioural changes observed in conscious animals. As a result of their many actions, adenosine analogues are being intensively investigated for use as anticonvulsant, anxiolytic, and neuroprotective agents.

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Factors affecting the release of purines from mouse cerebral cortex: Potassium removal and metabolic inhibitors

Cited by 9 publications

References 14 publications

In vivo release of [³H]‐purines by quinolinic acid and related compounds

In vivo release of [³H]‐purines by quinolinic acid and related compounds

Adenosine Release

Release and actions of adenosine in the central nervous system

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Factors affecting the release of purines from mouse cerebral cortex: Potassium removal and metabolic inhibitors

Cited by 9 publications

References 14 publications

In vivo release of [3H]‐purines by quinolinic acid and related compounds

In vivo release of [3H]‐purines by quinolinic acid and related compounds

Adenosine Release

Release and actions of adenosine in the central nervous system

Contact Info

Product

Resources

About

In vivo release of [³H]‐purines by quinolinic acid and related compounds

In vivo release of [³H]‐purines by quinolinic acid and related compounds