Characteristics of the release of adenosine from slices of rat cerebral cortex.

Hollins, Carolyn; Stone, T.W.

doi:10.1113/jphysiol.1980.sp013271

Cited by 51 publications

(18 citation statements)

References 35 publications

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“…The maximum efflux did not occur until 20 min after that of [3H]-noradrenaline efflux or contraction. The time course of 3H-purine efflux was nearly identical to that from the rat cerebral cortex slice described by Hollins & Stone (1980).…”

Section: Discusionsupporting

confidence: 73%

“…At high concentrations, KCI evokes a Ca2+-dependent purine efflux from various tissues, e.g., guinea-pig cerebral cortical synaptosomes (White, 1978;Potter & White, 1980) and rabbit vascular 0007-1188/82/120625-05 $01.00 adrenergic nerves (Katsuragi & Su, 1980;1982). Hollins & Stone (1980) found that ouabain (10-4M) as well as KCI elicited a Ca2+-dependent efflux of 3H-purines from rat cerebral cortex slices. The present study was, therefore, designed to compare the releasing effects of ouabain and high KCI on noradrenaline and purines with particular reference to their origins.…”

Section: Introductionmentioning

confidence: 99%

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Release of Purines and Noradrenaline by Ouabain and Potassium Chloride From Vascular Adrenergic Nerves

Katsuragi

1982

British J Pharmacology

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Release of [3H]‐noradrenaline and 3H‐purine by ouabain (10−4m) or high KCl (50 mm) was investigated in the superfused rabbit pulmonary arterial segment preincubated with [3H]‐noradrenaline or [3H]‐adenosine. Ouabain elicited a delayed large contraction and a parallel [3H]‐noradrenaline efflux. These were substantially inhibited by Ca2+‐free medium or preincubation with 6‐hydroxydopamine (30 μg/ml, 30 min). Ouabain caused an 3H‐purine efflux which was slower than the [3H]‐noradrenaline efflux. This was inhibited by 6‐hydroxydopamine and in part by phentolamine (3 × 10−6 m), indicating both neuronal and extraneuronal origins of purines. In contrast to ouabain, high KCl appeared to induce predominantly purine efflux, which was phentolamine‐insensitive and 6‐hydroxydopamine‐sensitive, indicative of neuronal origin. It is suggested that the purine efflux evoked by ouabain and high KCl may originate from different neuronal vesicles.

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Section: Discusionsupporting

confidence: 73%

Section: Introductionmentioning

confidence: 99%

Release of Purines and Noradrenaline by Ouabain and Potassium Chloride From Vascular Adrenergic Nerves

Katsuragi

1982

British J Pharmacology

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“…The Ca2+ dependency of ouabain-evoked release has been described previously (Hollins & Stone, 1980b With tissue from Wistar rats, morphine at 1 and 10JAM caused a small but significant elevation of ouabain-evoked purine release (Table-2). At both concentrations this effect could be blocked by naloxone, 0.1 or 1 JM.…”

Section: Resultsmentioning

confidence: 99%

“…However, previous examination of the characteristics of ouabain-evoked purine release was performed on tissue from rats only (Hollins & Stone 1980b) and it is possible that the properties of cortex slices important for ouabain-evoked release differ in rats and mice. We have concluded elsewhere that purine release by ouabain is probably not due to a simple inhibition of (Na+, K+) ATPase (Hollins, Stone & Lloyd, 1980;Stone, Hollins & Lloyd, 1981;.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Morphine and Methionine‐enkephalin on the Release of Purines From Cerebral Cortex Slices of Rats and Mice

Stone

1981

British J Pharmacology

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1 Slices of cerebral cortex from Wistar rats, TO mice or C57 mice were preincubated with [3H]-adenosine, and labelled purines were subsequently released by electrical stimulation or by perfusing with ouabain, 100 pM. 2 Electrically-evoked purine release was substantially reduced when the Ca2+ concentration in the medium was lowered from 2.4 to 0.1 mM. In both rats and mice, the electrically-evoked release was increased by morphine and methionine-enkephalin (Met-enkephalin), 10 fM and in rats and TO mice by morphine 1 Mm, both drug effects being prevented by naloxone. 3 Purine release evoked by ouabain was also increased by morphine 1 and 10 pM, though not by Met-enkephalin, from slices of rat cortex. Ouabain-induced release from TO mice was reduced by morphine, and from C57 mice was unchanged. 4 The enhancement by morphine of electrically-evoked purine release may indicate that purines mediate some effects of morphine in the CNS.

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“…Second, in CSD ATP is released extracellularly (Schock et al 2007), and this will be broken down to adenosine by ecto-ATPases. Third, in vivo CSD is thought to be initiated, at least in part, by elevated extracellular K ϩ (Vyskocil et al 1972), and K ϩ -induced depolarization also increases the extracellular adenosine concentration in various brain regions (Chen et al 1992;Van Wylen et al 1986) including cortex (Hollins and Stone 1980;Pazzagli et al 1994).…”

Section: Discussionmentioning

confidence: 99%

Cortical spreading depression-induced preconditioning in mouse neocortex is lamina specific

Gniel

Martin

2013

Journal of Neurophysiology

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Cortical spreading depression (CSD) is able to confer neuroprotection when delivered at least 1 day in advance of an ischemic event. However, its ability to confer neuroprotection in a more immediate time frame has not previously been investigated. Here we have used mouse neocortical brain slices to study the effects of repeated episodes of CSD in layer V and layer II/III pyramidal neurons. In layer V, CSD evoked at 15-min intervals caused successively smaller membrane depolarizations and increases in intracellular calcium compared with the response to the first CSD. With an inter-CSD interval of 30 min this preconditioning effect was much less marked, indicating that preconditioning lasts between 15 and 30 min. A single episode of CSD also provided a degree of protection in oxygen-glucose deprivation (OGD) by significantly lengthening the time a cell could withstand OGD before anoxic depolarization occurred. In layer II/III pyramidal neurons no preconditioning by CSD on subsequent episodes of CSD was observed, demonstrating that the response of pyramidal neurons to repeated CSD is lamina specific. The A1 receptor antagonist 8-cyclopentyl theophylline (8-CPT) reduced the layer V preconditioning in a concentration-related manner. Inhibition of extracellular formation of adenosine by blocking ecto-5'-nucleotidase with α,β-methyleneadenosine 5'-diphosphate prevented preconditioning in most but not all cells. Block of equilibrative nucleoside transporters 1 and 2 with dipyramidole alone or in combination with 6-[(4-nitrobenzyl)thio]-9-β-d-ribofuranosylpurine also prevented preconditioning in some but not all cells. These data provide evidence that rapid preconditioning of one CSD by another is primarily mediated by adenosine.

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Characteristics of the release of adenosine from slices of rat cerebral cortex.

Cited by 51 publications

References 35 publications

Release of Purines and Noradrenaline by Ouabain and Potassium Chloride From Vascular Adrenergic Nerves

Release of Purines and Noradrenaline by Ouabain and Potassium Chloride From Vascular Adrenergic Nerves

The Effects of Morphine and Methionine‐enkephalin on the Release of Purines From Cerebral Cortex Slices of Rats and Mice

Cortical spreading depression-induced preconditioning in mouse neocortex is lamina specific

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