Effect of hypoxia and glucose deprivation on ATP level, adenylate energy charge and [Ca2+]0-dependent and independent release of [3H]dopamine in rat striatal slices

doi:10.1016/0197-0186(95)00129-8

Neurochemistry International

Volume 28, Issues 5–6, May–June 1996, Pages 501-507

https://doi.org/10.1016/0197-0186(95)00129-8 Get rights and content

Abstract

Release of [³H]dopamine ([³H]DA) from rat striatal slices kept under hypoxic or/and glucose-free conditions was measured using a microvolume perfusion method. The corresponding changes in nucleotide content were determined by reverse-phase high-performance liquid chromatography (RPHPLC). The resting release of [³H]DA was not affected by hypoxia, but under glucose-free conditions massive [Ca²⁺]₀-independent release of [³H]DA was observed. Hypoxia reduced the energy charge (E.C.) and the total purine content from 19.36 ± 4.15 to 6.98 ± 1.83 mol/mg protein. Glucose deprivation by itself, or in combination with hypoxia, markedly reduced the levels of adenosine 5′-triphosphate (ATP), adenosine diphosphate (ADP) and adenosine monophosphate (AMP). The E.C. under glucose-free conditions was significantly reduced from 0.73 ± 0.04 to 0.44 ± 0.20. When the tissue was exposed to hypoxic and glucose-free conditions for 18 min the level of ATP was reduced to 3.15 ± 0.11 mol/mg protein. However, when the exposure time was 30 min the ATP level was further reduced to 1.11 ± 0.37 nmol/mg protein. The resting release was enhanced in a [Ca²⁺]₀-independent manner, but there was no release in response to stimulation, and tetrodotoxin did not affect the enhanced resting release, indicating that the release was not associated with axonal activity. Similarly, 50 μM ouabain, inhibitor of Na⁺/K⁺-activated ATPase, enhanced the release of [³H]DA at rest in a [Ca²⁺]₀-independent manner. It seems very likely that the reduced ATP level under glucose-free conditions leads to an inhibition of the activity of Na⁺/K⁺-ATPase that results in reversal of the uptake processes and in [Ca²⁺]₀-independent [³H]DA release from the axon terminals.

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Effect of hypoxia and glucose deprivation on ATP level, adenylate energy charge and [Ca2+]0-dependent and independent release of [3H]dopamine in rat striatal slices

Abstract

Brain Res.

Brain Res.

Neuroscience

Brain Res.

Neuroscience

J. biol. Chem.

Brain Res.

Neurosci. Lett.

Neuroscience

Progr. Neurobiol.

Neurochem. Int.

Neuroscience

Redistribution of glutamate and glutamine in slices of human neocortex exposed to combined hypoxia and glucose deprivation in vitro

J. Cereb. Blood Flow Metab.

External calcium independent release of neurotransmitters

J. Neurochem.

The energy charge of the adenylate pool as a regulatory parameter: interaction with feedback modifiers

Biochemistry

Biological differences between ischemia, hypoglycemia, and epilepsy

Ann. Neurol.

Elevation of the extracellular concentration of glutamate and aspartate in rat hippocampus during transient cerebral ischemia monitored by intracerebral microdialysis

J. Neurochem.

Cellular origin of endogenous amino acids released into the extracellular fluid of the rat striatum during severe insulin-induced hypoglycemia

J. Neurochem.

Excitatory and inhibitory effects of A1 and A2A adenosine receptor activation on the electrically evoked [3H]acetylcholine release from different areas of the rat hippocampus

J. Neurochem.

Effect of ischemia on the in vivo release of striatal dopamine, glutamate, and aminobutyric acid studied by intracerebral microdialysis

J. Neurochem.

Ischemia-induced shift of inhibitory and excitatory amino acids from intra- to extracellular compartments

J. Cereb. Blood Flow Metab.

Extracellular adenosine, inosine, hypoxanthine, and xanthine in relation to tissue nucleotides and purines in rat striatum during transient ischemia

J. Neurochem.

Effect of hypoxia and glucose deprivation on ATP level, adenylate energy charge and [Ca²⁺]₀-dependent and independent release of [³H]dopamine in rat striatal slices

Excitatory and inhibitory effects of A₁ and A_2A adenosine receptor activation on the electrically evoked [³H]acetylcholine release from different areas of the rat hippocampus