Brain amino acids during convulsions<sup>1</sup>

King, Lucy Jane; Carl, Juanita L.; Lao, Lauro

doi:10.1111/j.1471-4159.1974.tb11595.x

Cited by 13 publications

(2 citation statements)

References 7 publications

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“…Most intermediates, including those not measured, are at such low concentrations (Lowry et al, 1964;King et al, 1973) that even very large changes would have little effect on the size of the pool of intermediates (which includes the associated amino acids alanine, glutamate, glutamine, and aspartate). y-Aminobutyrate levels, not measured in our studies, do not change in cerebral cortex during the first 30 s after ECS or onset of bicucullineinduced seizures (King et al, 1974;Chapman et al, 1977). Thus, changes in brain lactate levels are a reasonable approximation of changes in the pool of intermediates of glucose metabolism and can be used, as we have done, in calculations of rates of glucose oxidation.…”

Section: Appendixmentioning

confidence: 49%

Cerebral Metabolic Responses to Electroconvulsive Shock and Their Modification by Hypercapnia

Miller

Shamban

Corddry

et al. 1982

Journal of Neurochemistry

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Brain glucose metabolism was studied in paralyzed, ventilated rats given electroconvulsive shock (ECS) under normocapnic and hypercapnic conditions. Brains were obtained with a freeze-blowing apparatus. Rates of glucose utilization were determined with [2-14C]glucose and [3H]deoxyglucose as tracers. In normocapnic rats, ECS caused a large increase in the rate of glycolysis to 5--6 mumol/g/min. Brain lactate levels increased three- to fourfold. The stimulation of glucose metabolism was reflected in decreased brain glucose 6-phosphate concentration as early as 2--3 s after ECS. There were significant decreases in brain glucose and glycogen levels at 20 and 30 s after ECS. The decreases in endogenous brain glucose accounted for most of the increases in glucose utilization measured isotopically, implying that influx of glucose from blood into brain did not increase greatly over these time periods. Animals made hypercapnic by respiration with 10% CO2 for 2 min prior to ECS were different in their metabolic responses to ECS in several ways. The increases in glycolytic rate and lactate content of brain were half of those found in normocapnic rats. Brain glycogen and glucose concentrations did not change significantly in the hypercapnic rats during seizure activity. Thus, hypercapnia lessened the stimulation of glycolysis caused by ECS, but increased net influx of glucose from blood to brain. The mechanisms of these effects of hypercapnia are uncertain, but it is postulated that the effect on glycolytic activity is due to the acidosis and that the effect on glucose transport is due to an increase in capillary surface area.

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Section: Appendixmentioning

confidence: 49%

Cerebral Metabolic Responses to Electroconvulsive Shock and Their Modification by Hypercapnia

Miller

Shamban

Corddry

et al. 1982

Journal of Neurochemistry

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“…They also strongly suggest that endogenous amino acids were being utilized as alternative substrates (Lewis et alt 1974). Although ammonia production was significantly higher in convulsing animals in these experiments, a causative role for ammonia in the initiation of hypoglycaemia seizures cannot be inferred, as seizures themselves are associated with increased cerebral ammonia production (King, Carl & Lao, 1974).…”

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confidence: 81%

The effects of hypoglycaemia on cerebral blood flow and metabolism in the new‐born calf.

Gardiner¹

1980

The Journal of Physiology

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SUMMARY1. The effects of insulin hypoglycaemia on cerebral blood flow and metabolism have been examined in unanaesthetized, unrestrained calves between 1 and 26 days after birth.2. Cerebral blood flow was measured with an inert gas technique using molecular hydrogen, and cerebral metabolism was quantified by determination of arteriocerebral venous (A -V) concentration differences for oxygen, glucose, lactate, pyruvate, acetoacetate, f-D-hydroxybutyrate and ammonia.3. During normoglycaemia the mean (A -V) difference for glucose was close to one sixth that of oxygen, on a molar basis. A small net loss of pyruvate from the brain was found, but there was no significant (A -V) difference for lactate. Arterial concentrations of acetoacetate and fl-D-hydroxybutyrate were low, and no utilization of ketone bodies by the brain was demonstrated.4. Moderate hypoglycaemia (arterial plasma glucose concentration 1-2 m-mole/l.) had no measurable effect on either cerebral blood flow or metabolism.5. During profound hypoglyeaemia (arterial plasma glucose concentration < I 0 m-mole/l.) cerebral glucose uptake was sufficient to account for only 56 % of the cerebral oxygen consumption. Cerebral oxygen consumption fell in comatose animals, but increased during hypoglyeaemic convulsions, as did cerebral blood flow.6. In day-old calves hypoglycaemia was associated with a rise in blood lactate concentration and uptake of lactate by the brain. 7. A net loss of ammonia by the brain was observed during hypoglycaemia in calves at all ages examined. The loss was greater in convulsing than in comatose animals.

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Ammonia

Benjamin

1982

Chemical and Cellular Architecture

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Brain amino acids during convulsions¹

Cited by 13 publications

References 7 publications

Cerebral Metabolic Responses to Electroconvulsive Shock and Their Modification by Hypercapnia

Cerebral Metabolic Responses to Electroconvulsive Shock and Their Modification by Hypercapnia

The effects of hypoglycaemia on cerebral blood flow and metabolism in the new‐born calf.

Ammonia

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Brain amino acids during convulsions1

Cited by 13 publications

References 7 publications

Cerebral Metabolic Responses to Electroconvulsive Shock and Their Modification by Hypercapnia

Cerebral Metabolic Responses to Electroconvulsive Shock and Their Modification by Hypercapnia

The effects of hypoglycaemia on cerebral blood flow and metabolism in the new‐born calf.

Ammonia

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About

Brain amino acids during convulsions¹