Selective alteration of neurotransmitter release by low oxygen in vitro

@article{Hirsch2004SelectiveAO,
  title={Selective alteration of neurotransmitter release by low oxygen in vitro},
  author={Joseph A. Hirsch and Gary E. Gibson},
  journal={Neurochemical Research},
  year={2004},
  volume={9},
  pages={1039-1049}
}
The potassium-stimulated release of acetylcholine, norepinephrine, serotonin, glutamate, and 4-aminobutyrate from superfused rat cortical slices was studied during hypoxia. A reduction in oxygen tensions from 603±6 to 22±2 mm Hg selectively altered the calcium-dependent efflux of these neurotransmitters, but did not change their calcium-independent release. The calcium-dependent release of [14C]acetylcholine decreased (39%), while that of glutamate increased (66%) and 4-aminobutyrate, [3H… 
Cytosolic-free calcium and neurotransmitter release with decreased availability of glucose or oxygen
TLDR
The data are consistent with the hypothesis that hypoxia and hypoglycemia increase cytosolic-free calcium, which stimulates the release of dopamine and glutamate, whose excessive release may lead to subsequent cellular damage postsynaptically.
Differential alteration of dopamine, acetylcholine, and glutamate release during anoxia and/or 3,4-diaminopyridine treatment
TLDR
Results are consistent with the hypothesis that hypoxia induces a presynaptic deficit that may underlie postsynaptic ischemic-induced changes and may be an effective approach to preventing hypoxic-induced damage.
New Considerations on the Neuromodulatory Role of Thiamine
TLDR
These data confirm earlier findings with oxythiamine on the calcium-mediated synaptic transmission of acetylcholine and support a possible neuromodulatory role for thiamine distinct from its actions as a cofactor during metabolic processes.
Cytosolic free calcium concentrations in synaptosomes during histotoxic hypoxia
TLDR
Results suggest that hypoxia-induced elevations of synaptosomal [Ca2]i are due to an inability of thesynaptosome to buffer entering calcium.
Dopamine and serotonin in rat striatum duringin vivo hypoxic-hypoxia
TLDR
The hypoxic-induced elevation of these two neurotransmitters during normoxia may be important in the production of hypoxic/ischemic-induced cell damage, and after repeated, mild hypoxic episodes or moderate hypoxia, the increases in rat striatal extracellular dopamine and serotonin continue even duringnormoxia.
Inosine induces presynaptic inhibition of acetylcholine release by activation of A3 adenosine receptors at the mouse neuromuscular junction
TLDR
The effect of inosine on spontaneous and evoked ACh release, the mechanism underlying its modulatory action and the receptor type and signal transduction pathway involved are investigated.
Hypoxia‐induced secretion of serotonin from intact pulmonary neuroepithelial bodies in neonatal rabbit
TLDR
It is suggested that hypoxia stimulates 5‐HT secretion from intact NEBs via inhibition of K+ channels, augmentation of Na+‐dependent action potentials and calcium entry through L‐type Ca2- channels, as well as by positive feedback activation of 5‐ HT3 autoreceptors.
Excitatory amino acid neurotoxicity.
TLDR
This work has shown that L-glutamate is accepted as the predominant fast excitatory neurotransmitter in the vertebrate brain.
Adrenergic and Glutamergic Receptor Gene Expression and Their Functional regulation in the Cerebral Cortex of Hypoxia Induced Neonatal Rats:Role of Oxygen,Epinephrine and Glucose Supplementation
TLDR
Increased Adrenergic Receptor Gene Expression in the Cerebral Cortex of Hypoxia Induced Neonatal Rats: Epinephrine, Glucose and Oxygen EffectsKerala Science Congress, CESS Thiruvananthapuram (January 29 31'1.2006).
An in vitro model of anoxic-induced damage in mouse brain
TLDR
Evidence is provided that anoxic induced increases in calcium may be pathophysiologically important and that reducing calcium entry postsynaptically may alleviate anoxic-induced changes and this model may prove useful in elucidating the molecular basis of these changes.
...
1
2
3
4
...

References

SHOWING 1-10 OF 42 REFERENCES
Superfused cerebral tissues in hypoxia: neurotransmitter and amino acid retention; labile constituents and response to excitation.
TLDR
Retention of norepinephrine and serotonin by the tissue, and their release into the superfusing medium during electrical stimulation, were found to persist during hypoxia, and total free amino acids increased, the major increase being in the quantity found in the superfuse medium.
Neurotransmitter Metabolism in Rat Brain Synaptosomes: Effect of Anoxia and pH
TLDR
Responses of synaptosomes to anaerobiosis are remarkably similar to the behavior of intact brain in hypoxia and ischemia, and neurotransmitter uptake systems are more sensitive to short periods of anaerOBiosis than are either the energy metabolism or ion transport.
Effect of hypoxia on tyrosine and tryptophan hydroxylation in unanaesthetized rat brain
The Tyrosine and tryptophan hydroxylase enzymes have been proposed as rate‐limiting steps in the biosynthesis of catecholamines and 5‐hydroxytryptamine (5‐HT), respectively; thus under normal
3,4-diaminopyridine alters acetylcholine metabolism and behavior during hypoxia.
TLDR
It is demonstrated that the hypoxic-induced deficits in ACh metabolism and behavior can be partially reversed by interaction with Ca++ homeostasis and the therapeutic usefulness of 3,4-DAP in the treatment of human metabolic encephalopathies remains to be evaluated.
Acetylcholine and oxidative metabolism in septum and hippocampus in vitro.
Effects of metabolic inhibitors on norepinephrine release from the perfused spleen of the cat.
TLDR
It is concluded that the energy requirements for the release of NE are not extensive and that release is not impaired in the absence of either oxidative or glycolytic metabolism.
INHIBITION OF STIMULATED CEREBRAL CORTEX RESPIRATION AND GLYCOLYSIS BY CHOLINOLYTIC DRUGS.
Functional and biochemical aspects of catecholamine metabolism in brain under hypoxia
Decreases in Amino Acid and Acetylcholine Metabolism During Hypoxia
TLDR
Any explanation of the brain's sensitivity to a decrease in oxygen availability must include the alterations in the metabolism of the amino acid neurotransmitters as well as ACh.
...
1
2
3
4
5
...