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Cerebral extracellular calcium activity in severe hypoglycemia : Relation to extracellular potassium and energy state
The changes in extracellular Ca2+ (Cae) and K+ (Ke) activities were studied in the rat brain during insulin-induced hypoglycemia. At about the time of onset of isoelectric EEG in severe insulin-induced hypoglycemia (300-g male Wistar rats under 70% N2O anaesthesia), there was an increase in Ke which, at ∼13 mM, was associated with a fall in Cae. Ke peaked at 48 ± 12 mM, and Cae at 0.18 ± 0.28 mM.
Noradrenaline Metabolism in Neocortex and Hippocampus Following Transient Forebrain Ischemia in Rats : Relation to Development of Selective Neuronal Necrosis
Abstract: Noradrenaline (NA) metabolism tn the neocortex and hippocampus was examined in rats atl 1, 24, and 48 h following 15 min of reversible forebrain ischemia. As assessed by the ratio of accumulated 3,4‐dihydroxyphenylalanine (DOPA) to the tissue NA level after inhibition of DOPA decarboxylase, the NA turnover rates were markedly increased (120‐148% above the control) at 1 h postischemia in
Excitatory amino acids and cerebrovascular tone
Levels of excitatory amino acids in the brain extracellular fluid compartment rise during pathological conditions in the brain such as ischaemia, anoxia and epilepsy. One such amino acid, glutamate, is present in sensory nerve fibres innervating, for example, cerebral vessels. Enhanced levels of circulating glutamate and aspartate are found in migraine sufferers. The present study examined whether
Pyruvate dehydrogenase activity in the rat cerebral cortex following cerebral ischemia
The effect of cerebral ischemia on the activity of pyruvate dehydrogenase (PDH) enzyme complex (PDHC) was investigated in homogenates of frozen rat cerebral cortex following 15 min of bilateral common carotid occlusion ischemia and following 15 min, 60 min, and 6 h of recirculation after 15 min of ischemia. In frozen cortical tissue from the same animals, the levels of labile phosphate compounds,
Dynamic changes of excitatory amino acid receptors in the rat hippocampus following transient cerebral ischemia
The changes in excitatory amino acid receptor ligand binding induced by transient cerebral ischemia were studied in the rat hippocampal subfields. Ten minutes of ischemia was induced by common carotid artery occlusion combined with hypotension, and the animals were allowed variable periods of recovery ranging from 1 day to 4 weeks. The binding of 3H-AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole
Protein kinase C is translocated to the plasma membrane during cerebral ischemia, but is partially inactivated
Cortical spreading depression is associated with arachidonic acid accumulation and preservation of energy charge
The present study aimed to study the relation between the release of arachidonic acid (AA) and the energy state in cerebral cortices of rats during single episodes of cortical spreading depression (CSD). The changes in concentrations of AA, labile phosphate compounds [ATP, ADP, AMP, and phosphocreatine (PCr)], and glycolytic metabolites (lactate, pyruvate, glucose, and glycogen) were studied durin
Mechanisms of glutamate neurotoxicity in cerebral ischemia
The NMDA-antagonist MK-801 reduces extracellular amino acid levels during hypoglycemia and prevents striatal damage
Protective effect of lesion to the glutamatergic cortico-striatal projections on the hypoglycemic nerve cell injury in rat striatum
In rat striatum severe hypoglycemia causes an irreversible nerve cell injury, which does not become manifest until during the post-insult recovery period. This injury can be ameliorated by lesions of the glutamatergic cortico-striatal pathway, which suggests that an "excitotoxic" effect mediated by the glutamatergic input is the likely cause of the posthypoglycemic nerve cell destruction. In this
Changes in Excitatory Amino Acid Receptor Binding in the Intact and Decorticated Rat Neostriatum Following Insulin‐Induced Hypoglycemia
Abstract: An involvement of excitatory amino acid (EAA) transmitter–receptor interactions in the development of hypoglycemia‐induced neuronal damage has been suggested. We report here on the binding to EAA receptors in the rat caudate nucleus and cerebral cortex, during and following severe insulin‐induced hypoglycemia with an isoelectric EEG of 10 or 30 min duration. The binding of α[3H]amino‐3‐h
Impairment of protein ubiquitination may cause delayed neuronal death
The hippocampus is a brain structure specifically vulnerable to short periods of transient cerebral ischemia, and which displays delayed neuronal necrosis. Protein ubiquitination is a posttranslational modification of proteins and an important factor in heat shock response and a regulator of ATP-dependent protein degradation. Using affinity purified antibodies against ubiquitin and ubiquitin-prote
Postischemic administration of idazoxan, an α-2 adrenergic receptor antagonist, decreases neuronal damage in the rat brain
The effect of an α-2 receptor antagonist, idazoxan, on ischemic neuronal damage in the hippocampus and neocortex was studied in rats following 10 min of forebrain ischemia. Idazoxan was given 0.1 mg/kg i.v. immediately after recirculation, followed by 48 h of continuous infusion at a rate of 10 μg/kg/min. A histopathological examination of the CA1 region of the dorsal hippocampus and neocortex fro
Excitatory amino acid receptors and ischemic brain damage in the rat
The excitatory amino acid glutamate has been suggested to be an important mediator of the selective CA1 hippocampal damage which follows transient cerebral ischemia. In order to evaluate the possible involvement of altered glutamate receptor regulation in the expression of the delayed neuronal necrosis following ischemia, we have determined the density of glutamate receptor subtypes in the rat hip
Effect of Insulin‐Induced Hypoglycemia on the Concentrations of Glutamate and Related Amino Acids and Energy Metabolites in the Intact and Decorticated Rat Neostriatum
Abstract The glutamate (Glu) terminals in rat neostriatum were removed by a unilateral frontal decortication. One to two weeks later the effects of insulin‐induced hypoglycemia on the steady‐state levels of amino acids [Glu, glutamine (Gin), aspartate (Asp), γ‐aminobutyric acid (GABA), tau‐rine] and energy metabolites (glucose, glycogen, α‐ketoglu‐tarate, pyruvate, lactate, ATP, ADP, AMP, phosphoc
Circulating catecholamines modulate ischemic brain damage
In search of factors influencing the outcome of an ischemic insult, we induced 10 min of forebrain ischemia in rats and assessed neuronal necrosis by quantitative histopathology after 1 week of recovery. Procedures for inducing ischemia included bilateral carotid artery clamping and reduction of blood pressure to 40–50 mm Hg by bleeding. To facilitate rapid lowering of blood pressure, a ganglionic
Lesions to the Corticostriatal Pathways Ameliorate Hypoglycemia‐Induced Arachidonic Acid Release
Abstract The concentrations of free fatty acids (FFAs) in the neostriatum of control rats and rats subjected to unilateral cortical ablation were measured during and following severe insulin‐induced hypoglycemia. The total FFA concentration in the caudate nucleus contralateral to the lesion increased to approximately 1.5 and 3 times the control level after 5 and 30 min of isoelectricity, respectiv