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strychnine/hypoxia
Nuoroda įrašoma į mainų sritį
Puslapis 1 nuo 38 rezultatus
[Action of strychnine and caffeine on the resistance of the cerebral cortex of the rat to experimental anoxia].
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Strychnine poisoning as an unusual cause of convulsions.
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A fatal case of strychnine poisoning is presented. The patient vomited then suffered a series of tonic convulsions which were triggered by tactile stimulation. In between paroxysms he was initially alert. Eventually the patient became comatosed due to anoxia and had a cardiac arrest. He presented
[Effect of cerebral hypoxia and hyperventilation hypocapnia on the epileptiform activity of the cerebral cortex of the cat].
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Influence of cerebral hypoxia and hyperventilatory hypocapnia on the ECoG and focal epileptiform activity of the cerebral cortex induced with local application of strychnine was studied in cats with transection of spinal cord at C1. Although both hypoxia and hypocapnia produced synchronization of
Glycine protects against hepatocyte killing by KCN or hypoxia by preventing intracellular Na+ overload in the rat.
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Glycine has been shown to prevent hepatocyte death induced by anoxia and by several toxic agents. However, the mechanisms responsible for such a cytoprotective effect have not yet been entirely clarified. We have previously shown that an uncontrolled increase in intracellular Na+ is critical for
Effects of anoxia on rat midbrain dopamine neurons.
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1. Dopamine-containing neurons of the rat midbrain were recorded intracellularly in vitro. Anoxia (2-5 min) caused reversible membrane hyperpolarization (4-25 mV), which blocked spontaneous firing of action potentials. Under voltage clamp, anoxia produced an outward current (100-1,000 pA) associated
Hydrogen sulfide mediates hypoxia-induced relaxation of trout urinary bladder smooth muscle.
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Hydrogen sulfide (H2S) is a recently identified gasotransmitter that may mediate hypoxic responses in vascular smooth muscle. H2S also appears to be a signaling molecule in mammalian non-vascular smooth muscle, but its existence and function in non-mammalian non-vascular smooth muscle have not been
Increase in brain prostaglandins during convulsions is due to increased neuronal activity and not to hypoxia.
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The levels of prostaglandin D2 (PGD2) and prostaglandin F2 alpha (PGF2 alpha), being the major prostaglandins formed in mouse brain in vivo were determined using a radioimmunological technique. Under basal conditions, they were less than 8.49 ng/g for PGD2 and less than 3.76 ng/g for PGF2 alpha.
Taurine activates glycine and GABAA receptor currents in anoxia-tolerant painted turtle pyramidal neurons.
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Unlike anoxia-intolerant mammals, painted turtles can survive extended periods without oxygen. This is partly accomplished by an anoxia-mediated increase in gamma-aminobutyric acid (GABA) release, which activates GABA receptors and mediates spike arrest in turtle neurons via shunting inhibition.
Facilitation of spontaneous glycine release by anoxia potentiates NMDA receptor current in the hypoglossal motor neurons of the rat.
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Deficiency in energy supply, such as occurs during hypoxia, anoxia, metabolic stress and mitochondrial failure, strongly affects the excitability of central neurons. Such lowered energy supply evokes various changes in spontaneous synaptic input to the hippocampal and cortical neurons. However, how
Facilitation of distinct inhibitory synaptic inputs by chemical anoxia in neurons in the oculomotor, facial and hypoglossal motor nuclei of the rat.
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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the selective loss of motor neurons in the brainstem and spinal cord. Clinical studies have indicated that there is a distinct region-dependent difference in the vulnerability of motor neurons. For example,
Modification of the glycine (co-activator) binding site of the N-methyl-D-aspartate receptor in the guinea pig fetus brain during development following hypoxia.
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The present study was designed to investigate the mechanism of NMDA receptor activation as a function of brain maturation by studying the development of the glycine binding site of the NMDA receptor and its modification by in-utero hypoxia in the guinea pig fetus brain during gestation. Measurements
Cytoprotection by glycine against hypoxia-induced injury in cultured hepatocytes.
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The aim of this study was to investigate the mechanism of cytoprotection by glycine against hypoxia-induced hepatocellular injury. Incubation under hypoxic conditions (95% N2 and 5% CO2) for 5 h induced about 50% cell death, but administration of glycine remarkably reduced hepatocellular death
Gasping is elicited by briefer hypoxia or ischemia following blockade of glycinergic transmission.
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The 'switching model' for generation of respiratory rhythms holds that gasping represents the release of a rostral medullary pacemaker mechanism from the pontomedullary neuronal circuit that generates eupnea. In a perfused preparation of the decerebrate juvenile rat, exposure to ischemia or
The role of glycine in anoxia/aglycaemia-induced potentiation of N-methyl-D-aspartate receptor-mediated postsynaptic potentials in the rat hippocampus.
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During brain ischaemia there is a sustained increase in extracellular glycine levels, and the potential role of these changes in modulating N-methyl-D-aspartate (NMDA) receptor-mediated activity following an anoxic/aglycaemic insult was studied in the rat hippocampal slice. Addition of large
Comparison of respiratory-related trigeminal, hypoglossal and phrenic activities.
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In decerebrate, paralyzed and vagotomized cats, we recorded activities of hypoglossal and phrenic nerves and of the mylohyoid branch of the trigeminal nerve. At normocapnia, a respiratory-modulated trigeminal discharge could be discerned in most cats. This discharge was characterized by a diminution
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