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)

Influenza viruses have been shown to decrease the ability of polymorphonuclear leukocytes (PMN) to respond to a variety of stimuli. This study was done to determine if viral neuraminidase was responsible for decreased PMN function. Treatment of human PMN with purified neuraminidases from influenza virus, Vibrio cholerae, or Clostridium perfringens did not significantly affect the ability of human PMN to respond to stimulation. Occasional virus preparations that lacked the ability to depress PMN function did not differ in neuraminidase activity from viruses capable of causing depression. These results demonstrate that neuraminidase activity is not the cause of influenza virus-induced PMN dysfunction.
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PMID:Neuraminidase activity is not the cause of influenza virus-induced neutrophil dysfunction. 286 60

Cultured NCB-20 hybrid cells express adenylate cyclase-coupled receptors for 5-hydroxytryptamine (5-HT) that correspond biochemically and pharmacologically to 5-HT1 receptors in rodent brain membrane preparations, apart from a much-reduced affinity for 5-HT (160 nM compared to less than 5 nM in brain). Since NCB-20 cells also differ from rodent brain both qualitatively and quantitatively in their ganglioside composition, the effects of exogenously added gangliosides on the affinity of the 5-HT1 receptor for 5-HT were tested. Both GM1 ganglioside (the cholera toxin receptor) and tetrasialoganglioside GQ1b produced a 10-fold increase in receptor affinity for [3H]5-HT, measured by binding studies. All gangliosides, at submicromolar concentrations, resulted in significantly reduced EC50 values for 5-HT-mediated elevation of intracellular cyclic AMP levels. GQ1b had the capacity to most dramatically enhance the potency of 5-HT in mediating increases in cyclic AMP levels. Gangliosides had no effect on the potency of DADLE or 3,4-dihydroxyphenylethylamine (dopamine)-mediated depression of cyclic AMP levels, suggesting some specificity for 5-HT. Our data are interpreted as implying a specific role for polysialogangliosides in modulating the affinity of the 5-HT1 receptor and the coupling of the 5-HT1 receptor-guanine nucleotide binding protein adenylate cyclase complex.
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PMID:Possible role of gangliosides in regulating an adenylate cyclase-linked 5-hydroxytryptamine (5-HT1) receptor. 299 94

Following removal of a skin patch from each hind limb of a series of adult newts, the limbs were explanted into small dishes of Holtfreter solution containing various combinations of test drugs. Later, the amount of wound epithelium that formed on each limb was determined using a planimeter on wound tracings obtained with the aid of a drawing tube-equipped microscope. Exposure of migrating cells to the plant lectin, concanavalin A (con A), lowered cyclic AMP (cAMP) levels and depressed migration. Exposure to cholera toxin and theophylline (CTX) significantly elevated cAMP levels and significantly depressed migration rate. Exposure of CTX-treated cells to con A tended to lower CTX-elevated cAMP levels while depressing the migration rate well beyond the depression caused by CTX alone. These results provide further evidence that cAMP can regulate the rate of newt epidermal cell migration. They also show that the inhibitory effect of con A on motility in these cells is independent of its effects on cAMP.
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PMID:Effects of concanavalin A and cholera toxin on epidermal cAMP and migration rate during wound closure in adult newts. 615 47

We have compared the effects of cellular cyclic AMP modulation on the regulation of lipoprotein lipase in cultures of rat epididymal pad preadipocytes and mesenchymal heart cells. Addition of dibutyryl cyclic AMP (dibutyryl cAMP) or 3-isobutyl-1-methylxanthine (IBMX) to preadipocytes grown in serum-containing culture medium resulted in a progressive decrease in lipoprotein lipase activity released into the culture medium so that at 6-8 h enzyme activity ranged between 20 and 30% of that recovered in the control dishes. Similar short-term (6-8 h) studies of the heart cell cultures showed a variable and much less pronounced depression of lipoprotein lipase activity. Thus, following dibutyryl cAMP and IBMX treatment, lipoprotein lipase activity ranged between 70 and 95% of control values. Incubation for 6 h with cholera toxin was followed by a 4-fold rise in the concentration of cellular cyclic AMP in both types of culture, but while in heart cell cultures enzyme activity was unchanged, lipoprotein lipase activity in preadipocytes decreased to 30% of control value. After 24 h incubation with all three effectors, an increase in lipoprotein lipase activity was seen. In the preadipocytes the increase ranged between 50 and 150% above control value, in the heart cell cultures it was 100-250%. 24-h incubation of heart cell cultures with dibutyryl cAMP resulted in a 6-fold increase of heparin-releasable lipoprotein lipase activity while residual activity was doubled. The rise in surface-bound lipoprotein lipase was evidenced also by an increase in the lipolysis of chylomicron triacylglycerol. In the presence of cycloheximide, the dibutyryl cAMP-induced heparin-releasable and residual lipoprotein lipase activity declined at the same rate as the basal activity. The reason for the difference in response of cultured preadipocytes and heart cells to the effectors during the first 8 h of incubation has not been elucidated, but could be related to a possible absence of hormone-sensitive lipase in the heart cells, and hence in a difference in intracellular metabolism of triacylglycerol. On the other hand, a common mechanism can be postulated for the long-term effect of cyclic AMP on the induction of lipoprotein lipase activity in both types of cultures. It probably involves mRNA and protein synthesis, which culminates in an increase in enzyme activity.
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PMID:Modulation of lipoprotein lipase activity in cultured rat mesenchymal heart cells and preadipocytes by dibutyryl cyclic AMP, cholera toxin and 3-isobutyl-1-methylxanthine. 618 19

The effect of a parasitic infection on enterotoxic diarrhea and on local and systemic formation of antibody to the toxin after immunization was studied in mice. Trichinella spiralis infection was chosen as the model, since the effects of the parasite when residing in both intestinal and extraintestinal sites can be studied. It was found that during the intestinal stage of the infection, the fluid response to cholera toxin as well as dibutyryl-cyclic adenosine 3',5' -monophosphate was greatly enhanced and that this was associated with a marked reduction in the absorption of fluid from the intestine. Later in the infection (migration stage), fluid accumulation in response to cholera toxin was significantly reduced, whereas absorption was normal and secretion in response to dibutyryl-cyclic adenosine 3',5'-monophosphate was somewhat increased. Still later in the infection (muscular stage), the fluid-secretory response to cholera toxin was normal. There was a drastic depression of local formation of antitoxin of both immunoglobulin and immunoglobulin classes in mice given the first two of four oral immunizations with cholera toxin during the intestinal stage of T. spiralis infection. When the priming was given before or after the intestinal stage, the local antitoxin response was not affected. The titers of circulating antibodies were also depressed in mice given the first immunizations during the intestinal stage. In addition, significant though less pronounced depression of the serum antibody response was observed in mice primed during the extraintestinal stage.
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PMID:Changes in intestinal fluid transport and immune responses to enterotoxins due to concomitant parasitic infection. 722 88

Turkeys inoculated with Pasteurella multocida either in the palatine air spaces or via drinking water were maintained t high (33.4-37.4 C), low (2.6-5.3 C), and moderate (19.8-22.4 C) temperatures in temperature-controlled chambers to determine the influence environmental temperature had on the pathogenesis of fowl cholera. In inoculated turkeys maintained at high temperatures, there was a delay in the onset of depression and, in most instances, in mortality in relation to those at low or moderate temperatures. In turkeys inoculated via drinking water and maintained at low temperatures, there was a higher mortality than in those at high or moderate temperatures. In turkeys maintained at low temperatures during the preinoculation period, the onset of depression was accelerated more after inoculation than in those maintained at moderate temperatures before inoculation. The percentage of leukocytes in the hematocrit was higher in turkeys inoculated int he palatine air spaces and maintained at low temperatures than in turkeys similarly inoculated but maintained at high or moderate temperatures. Cloacal temperatures were higher in all inoculated turkeys maintained at high temperatures than in those at low or moderate temperatures, and decreased markedly when turkeys became moribund. In turkeys inoculated in the palatine air spaces, deaths from pneumonia occurred more frequently at low temperatures and torticollis occurred more frequently at high temperatures than at the other temperatures.
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PMID:Effects of high and low environmental temperatures on clinical course of fowl cholera in turkeys. 727 40

Turkeys were hauled in a truck and exposed to Pasteurella multocida in the drinking water. The clinical course of fowl cholera was modified in hauled turkeys as compared to unhauled turkeys by delaying the onset of depression and reducing the severity of the disease. In unhauled turkeys, there was a marked increase in mortality in the first experiment and a marked increase in depression at the end of the second experiment. In both experiments average cloacal temperature was higher during the first 5 days after inoculation in unhauled than in hauled turkeys. On the day after hauling, plasma corticosterone concentration decreased in both hauled and unhauled turkeys.
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PMID:Influence of prior hauling on pathogenesis of Pasteurella multocida in turkeys. 732 6

Microinjecting cholinomimetics into the medial pontine reticular formation (mPRF) of conscious cats causes a rapid eye movement (REM) sleep-like state and state-dependent respiratory depression. Muscarinic receptors within the mPRF have been shown to mediate this state-dependent respiratory depression, but the specific signal transduction mechanisms remain poorly understood. This study tested the hypothesis that the cholinergically induced REM sleep-like state and state-dependent respiratory depression are mediated by guanine nucleotide binding proteins (G proteins). Cholera toxin, pertussis toxin, 5'-guanylylimidodiphosphate, and forskolin were microinjected alone and in combination with carbachol into the mPRF of intact unanesthetized cats. All of the G protein-altering compounds significantly reduced the ability of carbachol to produce the REM sleep-like state. Pertussis toxin caused the greatest decrease in the percent of time spent in the carbachol-evoked REM sleep-like state, showing for the first time mediation by a pertussis toxin-sensitive (Gi- or G(o)-like) G protein. Cholera toxin blocked the carbachol-induced respiratory depression, indicating mediation by a Gs-like G protein. Forskolin significantly decreased carbachol-evoked REM sleep. These data provide the first demonstration that adenylyl cyclase within the mPRF contributes to the carbachol induction of REM sleep and respiratory depression.
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PMID:Pertussis toxin-sensitive G proteins mediate carbachol-induced REM sleep and respiratory depression. 765 52

1. Rat cultured ventromedial hypothalamic (VMH) neurones obtained from embryonic hypothalamus were used to study the muscarinic (carbachol) modulation of voltage-gated K+ currents with the whole-cell patch-clamp technique. 2. Carbachol produced a potent and concentration-dependent (100 fM to 100 microM) decrease of the outward delayed rectifier K+ current (IK) with an IC50 of 44 pM and a Hill coefficient of 0.4. The carbachol-induced depression of IK was reduced by pirenzepine (1-10 microM) and atropine (1 microM). Carbachol had no effect on the transient outward K+ current (IA). 3. Intracellular dialysis with guanosine 5'-O-(2-thiodiophosphate) (GDP-beta-S, 500 microM) significantly diminished the carbachol-induced depression of IK, suggesting GTP-binding protein (G-protein) involvement. Pre-incubation of VMH neurones with pertussis toxin (200-400 ng ml-1) or cholera toxin (1 microgram ml-1) for 24-48 h had no effect on the carbachol-induced depression of IK. This suggested that the G alpha o, G alpha i, and G alpha s G-protein alpha-subunits were not involved in mediating the carbachol-induced depression of IK in VMH neurones. 4. Treatment (24-48 h) of VMH neurones with antisense phosphothio-oligodeoxynucleotides to the G alpha 11 G-protein subunit (10 microM) significantly diminished the carbachol-induced depression of IK. Treatment with 10 microM of either G alpha 11 sense or antisense to G alpha q had no effect. 5. These results demonstrate a novel and potent muscarinic depression of IK in VMN neurones, and that this depression is specifically mediated by the G alpha 11 G-protein subunit.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Muscarine modulation by a G-protein alpha-subunit of delayed rectifier K+ current in rat ventromedial hypothalamic neurones. 801 94

In July 1994, a small contingent of the French army had the physically and psychologically difficult task of burying 40,000 cadavers in Goma (Zaire). This was the only way to eradicate a cholera epidemic which decimated 1,200,000 Rwanda refugees fleeing from the war. The mission of the military psychiatrist posted in Goma consisted of promoting mental health actions and providing psychological support for the soldiers most "exposed" to the burial operations. He was unable to avoid a dozen sanitary evacuations (out of 200 soldiers), some of which were abusive, but discreetly helped the small proportion (25%) of soldiers determined to complete their mission despite the development of symptoms of anxiety, depression and personality disorders. The others assumed their task with no apparent difficulties. The solidarity of the military group (especially in the form of small units) and the hierarchical structure of the army enabled each member of the contingent to complete this dreadful task.
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PMID:[Psychological and psychiatric services provided to soldiers in the burial operation (Zaire, July-August 1994)]. 869 96


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