Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of intravenously injected 4-dimethylaminophenol and Co2EDTA on peripheral circulation, respiration, acid-base balance, and several other physiological and biochemical parameters were studied on dogs. DMAP increased the respiratory minute volume and mean arterial pressure, diminished the lactate-to-pyruvate ratio, and induced an increase in arterial oxygen pressure caused by liberation of oxygen from oxyhemoglobin during the formation of ferrihemoglobin. A study in vitro of the fate of the oxygen during the reaction between DMAP and oxyhemoglobin showed that only 30--40% of the oxygen released by the formation of ferrihemoglobin appeared in the gas phase. Co2EDTA caused circulatory depression, hyperventilation, and metabolic acidosis resulting in a decrease in base-excess and pH. The concentrations of lactate, pyruvate, potassium, and urea nitrogen and the hemoglobin content were increased by Co2EDTA. The side effects of Co2EDTA in therapeutic doses were more serious than those of DMAP. Thus the latter is superior in the therapy of cyanide poisoning, all the more since it detoxifies more cyanide.
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PMID:Effects of 4-dimethylaminophenol and Co2EDTA on circulation, respiration, and blood homeostasis in dogs. 11 Feb 89

Cyclic AMP (cAMP) was determined in that part of the rat cerebral cortex which was invaded by slow potential change (SPC) accompanying cortical spreading depression (CSD). cAMP was determined at various phases of SPC development and at several time intervals after SPC recovery. At maximum SPC, cAMP was increased by 100% above control and by 116% at the time of SPC recovery. Five, 10 and 15 min after SPC recovery, +54%, +34% and 0% increase in cAMP was found, respectively. The activity of phosphorylase a increased by 112% at SPC recovery (maximal cAMP increase), and by 13% 15 min later (complete cAMP recovery). Some depolarizing agents which differ in their ability to stimulate cAMP formation in vitro (veratridine, cyanide and glutamate) when applied topically onto the cerebral cortex in concentrations evoking CSD (2 mM veratridine, 10 mM cyanide and 100 mM glutamate), induced uniform increase of cAMP by about 100%. The same cAMP augmentation was found in the cortical region under maximum SPC induced by these agents.
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PMID:Brain cyclic adenosine 3',5'-monophosphate during depolarization of the cerebral cortical cells in vivo. 18 23

The specific activity of glutamine synthetase in cultured Chinese hamster cells is inversely related to the concentration of glutamine in the surrounding solution. Enzyme specific activity increases 8- to 10-fold when glutamine is removed from serum-free F12 growth media. The induction of glutamine synthetase activity occurs only after glutamine removal and not after the removal of other amino acids (methionine, leucine, or isoleucine). The analysis of the glutamine-mediated decrease in glutamine synthetase activity has been simplified by the finding that depression proceeds in nutrient-free buffered saline solution (141 mM NaCl, 5.4 mM KCl and 30 mM Tricine (pH 7.4). Under these conditions, 0.1 mM cyanide blocks glutamine-mediated depression. The cyanide inhibition is reversed by the addition of 1.0 mM glucose which suggests that ATP is required for depression. Glutamine-mediated depression is temperature-dependent, occurring between 25 and 45 degrees with an optimum rate at 37 degrees. Studies of the time course of induction and depression as a function of glutamine concentration suggest that glutamine regulates the rate at which the enzyme is either modified or degraded. We have employed an antibody prepared against homogeneous Chinese hamster liver glutamine synthetase to measure the amount of glutamine synthetase protein in extracts of cells containing induced or depressed levels of enzyme activity. A highly sensitive immunoprecipitation procedure enables quantitation of nanogram amounts of glutamine synthetase protein. Glutamine synthetase in cell extracts containing induced levels of enzyme activity possesses the same molecular specific activity (ratio of activity to antigenicity) as homogeneous Chinese hamster liver glutamine synthetase. The molecular specific activity of glutamine synthetase is almost the same in extracts of cells with depressed levels of enzyme obtained by growth for short (2 hours) and long (24 hours) times in the presence of glutamine. These data suggest that glutamine-mediated depression of glutamine synthetase results from degradation of enzyme molecules.
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PMID:Immunochemical evidence for glutamine-mediated degradation of glutamine synthetase in cultured Chinese hamster cells. 23 54

1. The effects of dopamine on the sensory discharges originating from arterial chemo- and baroreceptors were studied in vitro using carotid bodies or sinuses excised from anaesthetized cats and superfused with Locke's solution. 2. Intrastream injections of dopamine 10-200 mug produced a transient depression of the frequency of chemoreceptor discharges. This effect was observed in response to the first injection in eighteen out of twenty preparations. 3. The inhibitory effect of dopamine can counteract partially or totally the excitation of chemoreceptors evoked by simultaneous application of acetylcholine or cyanide. 4. This inhibitory effect of dopamine is reduced or abolished by pretreatment with dopaminergic (Spiroperidol) or alpha-adrenergic (Dibenamine) blockers. 5. In response to repeated injections of dopamine applied at short intervals, the inhibitory effect is replaced by a biphasic effect (early inhibition followed by late excitation), a late and long-lasting excitation or no changes in chemoreceptor activity. The late excitatory effects of dopamine are not blocked by dopaminergic or alpha-adrenergic blockers. 6. Noradrenaline does not affect the chemoreceptor activity of the superfused carotid body. DL-DOPA induces only a late and long-lasting excitatory effect. 7. In carotid sinus preparations, dopamine induces a weak but long-lasting increase in the frequency of baroreceptor discharges. 8. It is concluded that dopamine may play a modulatory role in the generation of chemoreceptor activity through local regulatory processes.
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PMID:Effects of dopamine on carotid chemo- and baroreceptors in vitro. 23 40

The mechanism of the 1'-4 coupling reaction between isopentenyl pyrophosphate and geranyl pyrophosphate catalyzed by farnesyl pyrophosphate synthetase from porcine liver was studied with the allylic substrate analogue 2-fluorogeranyl pyrophosphate. 2-Fluorogeranyl pyrophosphate is an alternate substrate for the enzyme, yielding 6-fluorofarnesyl pyrophosphate upon condensation with isopentenyl pyrophosphate. The Michaelis constant for the fluoroanalogue, Km = 1.1 micron, is similar to that measured for geranyl pyrophosphate, Km = 0.7 micron. However, the rate of condensation with the fluoroanalogue was only 8.4 X 10(-4) that of the normal reaction. A similar rate of depression (4.4 X 10(-3)) was found for solvolysis of geranyl methanesulfonate and the corresponding 2-fluoro derivative, reactions known to proceed via cationic intermediates. In contrast, displacement of chlorine from geranyl chloride and 2-fluorogeranyl chloride by cyanide showed a small (2-fold) rate enhancement for the fluoro compound. Finally, 2-fluorogeranyl pyrophosphate is a competitive inhibitor against geranyl pyrophosphate. These data are interpreted in terms of an ionization-condensation-elimination mechanism for the 1'-4 coupling reaction.
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PMID:Farnesyl pyrophosphate synthetase. Mechanistic studies of the 1'-4 coupling reaction with 2-fluorogeranyl pyrophosphate. 70 Dec 46

A technique is devised to determine the spatial distribution of the free ionized cytoplasmic calcium concentration ([Ca2+]i) inside a cell: Chironomus salivary gland cells are loaded with aequorin, and hte Ca2+-dependent light emission of the aequorin is scanned with an image-intensifier/television system. With this technique, the [Ca2+]i is determined simultaneously with junctional electrical coupling when Ca2+ is microinjected into the cells, or when the cells are exposed to metabolic inhibitors, Ca-transporting ionophores, or Ca-free medium. Ca microinjections elevating the [Ca2+]i in the junctional locale produce depression of junctional membrane conductance. When the [Ca2+]i elevation is confined to the vicinity of one cell junction, the conductance of that junction alone is depressed; other junctions of the same cell are not affected. The depression sets in as the [Ca2+]i rises in the junctional locale, and reverses after the [Ca2+]i falls to baseline. When the [Ca2+]i elevation is diffuse throughout the cell, the conductances of all junctions of the cell are depressed. The Ca injections produce no detectable [Ca2+]i elevations in cells adjacent to the injected one; the Ca-induced change in junctional membrane permeability seems fast enough to block appreciable transjunctional flow of Ca2+. Control injections of Cl- or K+ do not affect junctional conductance. The Ca injections that elevate [Ca2+]i sufficiently to depress junctional conductance also produce under the usual conditions an increase in nonjunctional membrane conductance and, hence, depolarization. But injections that elevate [Ca2+]i at the junction while largely avoiding nonjunctional membrane cause depression of junctional conductance with little or no depolarization. Moreover, elevations of [Ca2+]i in cells clamped near resting potential produce the depression, too. On the other hand, complete depolarization in K medium does not produce the depression, unless accompanied by [Ca2+]i elevation. Thus, the depolarization is neither necessary nor sufficient for depression of junctional conductance. Treatment with cyanide, dinitrophenol and ionophores X537A or A23187 produces diffuse elevation of [Ca2+]i associated with depression of junctional conductance. Prolonged exposure to Ca-free medium leads to fluctuation in [Ca2+]i where rise and fall of [Ca2+]i correlate respectively with fall and rise in junctional conductance.
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PMID:Permeability of a cell junction and the local cytoplasmic free ionized calcium concentration: a study with aequorin. 78 27

There was rapid efflux of L-leucine, L-phenylalanine, and alpha-methyl-D-glucoside after infection of Salmonella typhimurium with the clear plaque mutant C1 of phage P22. The efflux was similar to that observed with cyanide or arsenate treatment except that there was partial recovery in the case of phage infection and almost complete recovery under the condition of lysogeny. There was no efflux after infection with the temperature-sensitive mutant ts16C1 at nonpermissive temperature. Superinfection of superinfection exclusion negative lysogen (sie A minus sie B minus) with C1 led to efflux, whereas the efflux was much less on superinfection of sie A+ Sie B+ lysogen. These results indicate that an effective injection process is enough to cause depression in the cellular transport processes.
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PMID:Transport in bacteriophage P22-infected Salmonella typhimurium. 109 32

The intensity of oxygen consumption, as well as phospholipid metabolism of minced rat brain tissue were studied at different temperature of the incubation media (37 degrees, 32 degrees and 27 degrees C) without cyanide and in the media containing KCN (0.5 and 1.0 mM). As shown, both parameters depended directly upon the incubation temperature within the range of 27 degrees-37 degrees. KCN inhibited both processes, but depression of phospholipid metabolism was more expressed. These data suggest that under conditions of cyanide poisoning phospholipid metabolism depends both on the toxic effect of KCN directly and on the temperature, whose reduction reinforces this effect.
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PMID:[Intensity of respiration and the metabolism of phospholipids in isolated brain tissues of rats at various temperatures in the presence of KCN]. 119 69

Microinjections of cyanide (300 pmol) into the cardiovascular portion of the rostral ventrolateral reticular nucleus (RVL) of anesthetized rats (paralyzed and ventilated) produced a pressor response (26.5 +/- 1.6 mmHg, n = 7) and a transient depression of phrenic nerve discharge (90 +/- 8%, n = 5). Microiontophoretic applications of cyanide (less than or equal to 100 nA, 5-40 s) excited the RVL-spinal sympathoexcitatory neurons (31 out of 31). The response was dose dependent, reversible, independent of the baroreflex input to these neurons, and different from the responses of units with spontaneous discharge synchronized with the lung inflation or with unidentified function. The cyanide-induced excitation of the RVL-spinal sympathoexcitatory neurons was reversibly abolished by CO2+, applied iontophoretically at a dose at which the baroreflex inhibition of these neurons was not markedly affected whereas iontophoretic applications of kynurenic acid, a glutamate receptor antagonist, did not alter the response of the RVL-spinal sympathoexcitatory neurons to cyanide. It was concluded that cyanide induces a rapid Ca(2+)-dependent response of the RVL-spinal sympathoexcitatory neurons, which may underlie the cellular mechanism of these neurons in responding to ischemia-hypoxia.
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PMID:Cyanide excites medullary sympathoexcitatory neurons in rats. 153 25

1. The effects of brief exposures to hypoxia on the membrane currents of isolated hippocampal CA1 neurons were studied with the use of the whole-cell variation of the patch-clamp technique. Neurons were acutely dissociated from immature (day 2-7) and mature (day 21-43) rats. 2. In the current-clamp mode, Na-cyanide (CN) hyperpolarized both mature and immature neurons. In the voltage-clamp mode, CN decreased the magnitude of the hyperpolarizing holding current in both age groups. 3. CN did not have a consistent effect on the voltage-dependent calcium and potassium currents of immature and mature CA1 neurons but decreased the voltage-dependent inward current of neurons at both ages. This effect was age dependent: the inward current of immature neurons decreased by only 10%, but that of mature neurons decreased by approximately 40%. 4. The decrease in the magnitude of the hyperpolarizing holding current and the depression of the voltage-dependent inward current of mature neurons were observed during brief exposure to N2 (PO2 = 0), indicating that the electroresponses observed with CN were the result of blocking oxidative respiration. 5. The hypoxia-sensitive inward current was blocked by tetrodotoxin (TTX) but was not blocked by cadmium or cesium + tetraethylammonium (TEA). Therefore this current was identified as the voltage-dependent, fast-inactivating sodium current (INa). 6. The isolated sodium current was studied with the use of cadmium to block calcium and TEA + cesium to block potassium currents. In mature neurons, CN left-shifted the steady-state inactivation curve for INa and slowed the deactivation kinetics of INa. CN caused little or no change in INa activation, fast inactivation, recovery from inactivation, or current-voltage (I-V) relationship. 7. We conclude that brief exposures to CN and hypoxia alter the intrinsic excitability of CA1 neurons by at least two mechanisms: 1) alterations in leakage currents and 2) alterations in the fast Na+ conductance that are maturationally dependent. We propose that the alterations in the Na+ conductance may play an adaptive role by reducing O2 demands and thus possibly delaying neuronal injury.
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PMID:Effect of metabolic inhibition on the excitability of isolated hippocampal CA1 neurons: developmental aspects. 166 12


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