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glutamic acid decarboxylase/хипоксия
Линкът е запазен в клипборда
Страница 1 от 24 резултата
Permanent increase of immunocytochemical reactivity for gamma-aminobutyric acid (GABA), glutamic acid decarboxylase, mitochondrial enzymes, and glial fibrillary acidic protein in rat cerebral cortex damaged by early postnatal hypoxia-ischemia.
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A former study indicated that hypoxic-ischemic encephalopathy in rat sustained during early postnatal life may result in permanent epileptic activity in the baseline electroencephalogram. We, therefore, investigated whether the presumed higher firing frequency and metabolic activity of neurons in
Post-translational modification of glutamic acid decarboxylase 67 by intermittent hypoxia: evidence for the involvement of dopamine D1 receptor signaling.
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Intermittent hypoxia (IH) associated with sleep apnea leads to cardio-respiratory morbidities. Previous studies have shown that IH alters the synthesis of neurotransmitters including catecholamines and neuropeptides in brainstem regions associated with regulation of cardio-respiratory functions.
Hypoxia regulates the level of glutamic acid decarboxylase enzymes and interrupts inhibitory synapse stability in primary cultured neurons.
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Gamma-aminobutyric acid (GABA) is the main neurotransmitter of inhibitory synaptic transmission, which is critical for oscillatory activity and synchronization of neurons in neural networks. GABA is synthesized by glutamic acid decarboxylase (GAD) enzymes in the inhibitory neuron and, thus, the
Chronic hypoxia in rats: alterations of striato-nigral angiotensin converting enzyme, GABA, and glutamic acid decarboxylase.
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Developmental changes of glutamate acid decarboxylase-67 in mouse brain after hypoxia ischemia.
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Objective To study the developmental changes of glutamic acid decarboxylase-67 (GAD-67, a GABA synthetic enzyme) in normal and hypoxic ischemic (HI) brain. Methods C57/BL6 mice on postnatal day (P) 5, 9, 21and 60, corresponding developmentally to premature, term, juvenile and adult human brain were
Glutamic acid decarboxylase in cerebrospinal fluid in infancy and childhood. Part I. Glutamic acid decarboxylase activity in cerebrospinal fluid of normal infants and children.
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Glutamic acid decarboxylase (GAD) activity in the cerebrospinal fluid (CSF) of normal infants (n:14) and children (n:28) was determined by measuring the amount of 14CO2 released from L-[1-14C]-glutamic acid. The mean GAD activity in CSF of infants and children was 5.2 +/- 2.5 pmol CO2 formed/hr/ml.
Comparative Study on the Bread Making Quality of Normoxia- and Hypoxia-Germinated Wheat: Evolution of γ-Aminobutyric Acid, Starch Gelatinization, and Gluten Polymerization during Steamed Bread Making.
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To explore the bread making characteristics of germinated wheat flour, the current study focused on the componential evolution throughout the steamed bread making process. Hypoxia-germinated wheat (HGW) dough produced the maximum γ-aminobutyric acid as a result of high glutamic acid decarboxylase
Increased binding of [3H]muscimol and [3H]flunitrazepam in the rat brain under hypoxia.
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We examined the effects of in vivo hypoxia (10% O2/90% N2) on the gamma-aminobutyric acid (GABA)/benzodiazepine receptors and on glutamic acid decarboxylase (GAD) activity in the rat brain. Male Wistar rats were exposed to a mixture of 10% O2 and 90% N2 in a chamber for various periods (3, 6, 12,
Quantitative immunofluorescence data suggest a permanently enhanced GAD67/GAD65 ratio in nerve endings in rat cerebral cortex damaged by early postnatal hypoxia-ischemia: a comparison between two computer-assisted procedures for quantification of confocal laser scanning microscopic immunofluorescence images.
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The aim of the present study was 2-fold: (1) to determine the ratio between the amount of GAD67 and GAD65 (two isoforms of the GABA synthetizing enzyme glutamic acid decarboxylase) in nerve endings in the mature rat cerebral cortex damaged by hypoxia-ischemia during early postnatal life; and (2) to
[Effects of exogenous gamma-aminobutyric acid on polyamine metabolism of melon seedlings under hypoxia stress].
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Taking melon cultivar 'Xiyu No. 1 ' as test material, a hydroponic experiment was conducted to investigate the effects of exogenous gamma-aminobutyric acid (GABA) on the seedlings polyamine metabolism under hypoxia stress. Compared with the control in normoxic treatment, the seedlings under hypoxia
Hypobaric hypoxia modulates brain biogenic amines and disturbs sleep architecture.
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Sojourners to high altitude experience poor-quality of sleep due to hypobaric hypoxia (HH). Brain neurotransmitters are the key regulators of sleep wakefulness. Scientific literature has limited information on the role of brain neurotransmitters involved in sleep disturbance in HH. The present study
Effect of pre- and post-treatments with diazepam on the rat brain GABAergic system during anoxic stress and recovery.
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Anoxia induced by exposure to N(2) gas for 15, 30, 50 and 60 s showed appearance of varying degrees of restlessness, tremor and convulsive behaviour resulting in mortality of adult rats. Diazepam treatment in pre- and post-anoxic conditions (10 and 20 mg/kg, respectively) has been found to decrease
Spontaneous dorsal root potentials arise from interneuronal activity in the isolated frog spinal cord.
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Spontaneous dorsal root potentials (sDRPs) were recorded from the dorsal roots of the isolated frog spinal cord using sucrose gap techniques. sDRPs were always negative (depolarizing) in sign and ranged in size from about 100 microV to 6.0 mV. The largest sDRPs were 25-40% of the amplitude of DRPs
Effect of Plasmodium yoelii infection on GABA metabolism of mouse brain.
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Plasmodium yoelii infection in albino mice decreased the activity of brain glutamic acid decarboxylase (GAD) by about 30 and 48% in crude homogenate and its synaptosomal fraction, respectively. The decrease was evident from 20% parasitemia and remained more or less constant up to 80% parasitemia.
Induced cerebral hypothermia reduces post-hypoxic loss of phenotypic striatal neurons in preterm fetal sheep.
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Perinatal hypoxic-ischemic injury of the basal ganglia is a significant cause of disability in premature infants. Prolonged, moderate cerebral hypothermia has been shown to be neuroprotective after experimental hypoxia-ischemia; however, it has not been tested in the preterm brain. We therefore
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