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picrotoxin/hypoxia
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Effect of picrotoxin on organism's resistance to acute severe hypoxia.
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Organism's resistance to acute severe hypoxia (3% O2) was studied after administration of GABA(A) receptor antagonist picrotoxin and adenosine receptor antagonist euphylline (aminophylline) and after neutralization of secondary hypocapnia by adding 7% CO2 to the hypoxic mixture. Administration of
Experimental evaluation of drugs for coronary insufficiency induced by hypoxemia and picrotoxin.
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The Hypoxia Mimetic Protocatechuic Acid Ethyl Ester Inhibits Synaptic Signaling and Plasticity in the Rat Hippocampus.
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During hypoxia a number of physiological changes occur within neurons including the stabilization of hypoxia-inducible factors (HIFs). The activity of these proteins is regulated by O2, Fe2+, 2-OG and ascorbate-dependant hydroxylases which contain prolyl-4-hydroxylase domains (PHDs). PHD inhibitors
[Changes in mitochondria energy function under the effect of eserine and picrotoxin].
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Intoxication caused by intramuscular injection of picrotoxin and eserine (5 and 10 mg/kg) to albino rats is found to increase the degree of coupling of oxidation to phosphorylation and the rate of succinate oxidation. The conclusion may be drawn that the reaction of the oxidative phosphorylation
Hypoglossal and phrenic nerve responses to changes in oxygen tension during picrotoxin-induced seizures in the rat.
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The aim of this study was to examine the response of phrenic and hypoglossal motor outputs to hyperoxia and 11% hypoxia during picrotoxin-induced seizures. Adult rats were anesthetized with a mixture of urethane with alpha-chloralose. The animals were bilaterally vagotomized, paralyzed, and
[Changes in individual resistance of cardiovascular and respiratory systems of rats to posthemorrhagic hypoxia after pharmacological impact on brain function].
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In experiments on rats it was shown that injection to rats before hemorrhage of analeptic corasol or prior injections during three days of the inhibitory mediator sodium oxybutyrate decrease individual resistance of the respiratory and circulatory systems (arterial blood pressure, cardiac output,
Mechanism of early anoxia-induced suppression of the GABAA-mediated inhibitory postsynaptic current.
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1. We investigated the mechanism of hypoxia-induced depression of gamma-aminobutyric acid-A (GABAA)-mediated inhibitory postsynaptic currents (IPSCs) in CA1 neurons of hippocampal slices from 21- to 28-day-old rats. Cells were examined by whole-cell patch-clamp recording and hypoxia was induced by
[Respiratory and cardiovascular responses to hypoxia under activation or blockade inhibitory transmission].
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Respiratory rhythm changes and hypoxic ventilatory responses were studied in anesthetized albino rats after administration GABA and adenosine receptor antagonists. Intracisternal microinjection of picrotoxin induced pathological periodic breathing. Picrotoxin intravenous administration caused the
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,
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 synthesis of prostaglandins and thromboxane in the mouse brain in vivo. Influence of drug induced convulsions, hypoxia and the anticonvulsants trimethadione and diazepam.
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1. The i.v. administration of convulsant doses of penetrazole or picrotoxin induced an increase in PGF2 alpha, PGE2 and TXB2-like immunoreactive material in mouse brain tissue. The onset of increase coincided with the appearance of clonic seizures. 2. The anticonvulsant drugs trimethadione and
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
Resuscitation of the newborn.
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All infants have some degree of hypoxia and respiratory acidosis at birth, but these conditions are more profound in the asphyxiated newborn. The newborn infant is very susceptible to cooling and may require warming. Skin temperature should be maintained between 36-36.5 degrees .(2) Resuscitation of
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