Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0043167 (pertussis)
19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The involvement of a GTP-binding protein (G-protein) in the process of neurotransmitter release was examined using pertussis toxin and cholera toxin. Cholinergic agonists are shown to mediate [3H]noradrenaline release in rat brain slices via a pertussis toxin (1.2 micrograms/ml) sensitive, and cholera toxin (0.5 microgram/ml) insensitive G-protein. An indication for the involvement of a G-protein and phospholipase C activation in the release process was implied from the inhibitory effect of neomycin on K+-, veratridine- and carbachol-induced-norepinephrine release. Depolarizing agents mediate a neomycin-sensitive release, which is not which is not affected either by pertussis toxin or cholera toxin, suggesting a different mode of phospholipase C activation, unlike carbachol-induced release, which is both neomycin and pertussis toxin sensitive. Similarly, a hormone-sensitive carrier activated by phenylephrine not via alpha 1-adrenergic receptors, mediates a non-exocytosis efflux which is not affected by neomycin and is shown to be pertussis toxin-insensitive. The inhibitory action of protein kinase C inhibitors polymyxin B, K252a and H-7 [(1-(5-isoquinolinesulphonyl)-2-methyl-piperazine] on release, strongly suggests its participation in the process. Polymyxin B, a relatively selective protein kinase C inhibitor, inhibited carbachol-induced release (IC50 = 0.53 microM) as well as the K+ and the veratridine induced [3H] noradrenaline release, K252a, an inhibitor of various protein kinases at the ATP site, and H-7, another protein kinase C inhibitor, inhibited carbachol-induced noradrenaline released with IC50 = 35 nM and 3 microM respectively. Consistent with its inability to activate phospholipase C, phenylephrine-induced noradrenaline efflux was unaffected by polymyxin B (greater than 70 microM). These results offer more supportive evidence for a major role played by the dual messengers inositol trisphosphate and diacylglycerol (IP3/DG) in the mechanisms of neuronal release.
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PMID:Cholinergic-induced [3H] noradrenaline release in rat brain cortical slices is mediated via a pertussis toxin sensitive GTP binding protein and involves activation of protein kinase C. 251 86

Norepinephrine (NE) stimulated FRTL-5 thyroid cells via an alpha 1-adrenergic receptor, resulting in cytosolic Ca2+ [( Ca2+]i) mobilization and activation of phospholipase C. Adenosine and its receptor agonist, phenylisopropyladenosine (PIA), although not exerting a direct effect, markedly enhanced the NE-induced changes. Basal NE action was not totally abolished whereas the permissive action of adenosine and PIA was completely abolished by pretreatment of the cells with islet-activating protein (IAP), pertussis toxin. The decrease in cAMP level induced by adenosine or PIA is not the cause of their permissive effect, since the effect was not reversed by the addition of cAMP-increasing agents. We conclude that an IAP substrate GTP-binding protein(s) plays a novel role in forming a stimulatory coupling between an adenosine receptor and an alpha 1-adrenergic receptor-coupled phospholipase C system.
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PMID:Stimulation of adenosine receptor enhances alpha 1-adrenergic receptor-mediated activation of phospholipase C and Ca2+ mobilization in a pertussis toxin-sensitive manner in FRTL-5 thyroid cells. 254 83

Noradrenaline- and clonidine-induced inhibition of insulin release from intact and electrically permeabilized rat islets was markedly relieved by prior exposure to 100 ng of Bordetella pertussis toxin/ml. The reversal of catecholamine inhibition of insulin secretion by this toxin was not associated with a decrease in specific binding of the alpha 2-adrenergic ligand [3H]yohimbine, and could not be fully explained by an increase in intracellular cyclic AMP. Exposure of intact islets to 1 microgram of pertussis toxin/ml for 2 h, followed by electrical permeabilization and incubation with 5 microCi of [alpha-32P]NAD+, resulted in the ADP-ribosylation in situ of a protein of molecular mass approx. 41 kDa. These results suggest that pertussis toxin alleviates catecholamine inhibition of beta-cell secretory responses by ADP-ribosylating at least one protein of molecular mass 41 kDa. In analogous systems the 41 kDa substrate of pertussis toxin has been shown to be the alpha subunit of Gi, but catecholamine-activated G proteins linked to effector systems other than adenylate cyclase might also be modified by this toxin in pancreatic beta-cells.
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PMID:Effects of Bordetella pertussis toxin on catecholamine inhibition of insulin release from intact and electrically permeabilized rat islets. 254 59

Opioid agonists selective for mu-, delta-, and kappa-receptors are all capable of regulating the stimulated release of noradrenaline from three terminal fields (cortex, hippocampus, and cerebellum) of the noradrenergic projections from locus coeruleus in the guinea pig brain. Intracerebroventricular injections of pertussis toxin abolished the ability of a mu-selective agonist and of a delta-selective agonist to inhibit stimulated noradrenaline release, but left unaffected the concentration-related inhibition of NE release by a kappa agonist. Thus, mu- and delta-receptors have been shown to be coupled to their effector system in these noradrenergic neurons via guanyl nucleotide binding proteins (G proteins) which are sensitive to pertussis toxin, while kappa-receptors in the same neurons appear to be coupled through a different mechanism which is significantly less sensitive to pertussis toxin. In contrast to opioid receptor regulation of noradrenaline release in guinea pig hippocampus, mu-, but not delta- or kappa-agonists are capable of regulation of stimulated noradrenaline release from rat hippocampus and cortex, and kappa-, but not mu- or delta-agonists are capable of inhibiting the stimulated release of dopamine from rat striatum and cortex. Pertussis toxin injections significantly attenuated mu-agonist inhibition of noradrenaline release, but had no effect on the ability of a kappa-selective agonist to regulated dopamine release, confirming the insensitivity of the kappa-receptor-effector coupling system to pertussis toxin.
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PMID:Effects of pertussis toxin on opioid regulation of catecholamine release from rat and guinea pig brain slices. 254 29

In dissociated neurons of rat superior cervical ganglion (SCG), noradrenaline (NA) and acetylcholine (ACh) suppressed Ca2+ currents elicited by depolarizations to 0 mV from -60 mV. With GTP-gamma-S in patch electrodes, ACh and NA caused persistent inhibition of Ca2+ currents. Pretreatment of SCG cells with pertussis toxin abolished the action of ACh but not of NA. The results suggest that ACh and NA reduce the Ca2+ currents in SCG cells through different G proteins.
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PMID:Different GTP-binding proteins mediate regulation of calcium channels by acetylcholine and noradrenaline in rat sympathetic neurons. 255 Jan 9

In order to examine the involvement of G-proteins in mediating the different effects of adenosine A1-receptor stimulation in rat hippocampus we injected pertussis toxin (PTX) intraventricularly close to the hippocampus and examined its effect in slices 48-60 h later. The in vivo PTX treatment caused a partial (50 +/- 5%) inhibition of the [32P]ADP ribosylation produced by PTX added together with [32P]NAD in vitro. Such PTX treatment eliminated the electrophysiologically determined gamma-amino-n-butyric acid (GABA)B receptor response in the hippocampal CA1 region, but GABAA effects were unaffected. The adenosine (50 microM)-mediated hyperpolarization and decrease in input resistance as well as the adenosine-mediated inhibition of low calcium-induced bursting in pyramidal CA1 neurons were virtually abolished. The same was true for the decrease in [3H]cyclic AMP accumulation that is produced by the adenosine analogue R-N6-phenylisopropyl adenosine (R-PIA) in forskolin-treated hippocampal slices. As far as modulation of transmitter release was concerned, the R-PIA (1 microM)-induced inhibition of release of both [3H]noradrenaline (NA) and [3H]acetylcholine (ACh) evoked by field stimulation in hippocampal slices was affected hardly or not at all by pertussis toxin treatment. The inhibitory effect of adenosine on field excitatory postsynaptic potential (EPSP)s evoked in the CA1 region was unaltered by PTX pretreatment. The present results show that in vivo pertussis toxin treatment can inhibit some but not all A1-adenosine-receptor effects. This strongly suggests that closely similar A1 receptors might be coupled to G-proteins that differ in their sensitivity to PTX treatment.
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PMID:In vivo pertussis toxin treatment attenuates some, but not all, adenosine A1 effects in slices of the rat hippocampus. 255 Feb 63

We demonstrated previously that alpha-1 adrenergic catecholamines modulate cardiac automaticity in a manner that is dependent upon the function of a pertussis toxin sensitive guanine nucleotide binding protein (G protein). Furthermore, we demonstrated that alpha-1 adrenergic receptor stimulation promotes the accumulation of inositol monophosphate (IP1). In the present study we used high-pressure liquid chromatography to resolve individual inositol phosphate isomers formed in norepinephrine-stimulated cultured rat ventricular myocytes. Norepinephrine stimulated a rapid, transient increase in 1,4,5-inositol trisphosphate (1,4,5-IP3) which was followed by slower, sustained increases in 1,3,4-IP3, inositol bisphosphate (IP2) and IP1. IP1 was composed of two major isomers with retention times characteristic of 1-IP1 and 4-IP1. 4-IP1 was the predominant IP1 isomer formed during stimulation with norepinephrine suggesting that the polyphosphoinositides rather than phosphatidylinositol are the principal targets of norepinephrine-stimulated phospholipase C activity in the heart. This was confirmed in studies performed on myocyte membranes which demonstrated proportionately greater IP2 and IP3 (relative to IP1) accumulation in response to norepinephrine. G protein regulation of alpha-1 adrenergic-dependent inositol phospholipid hydrolysis also was examined. In myocyte membranes, guanosine-5'-0-(3-thiotriphosphate) induced the accumulation of IP2 and IP3 and was required for the stimulatory effect of norepinephrine. This response was not impaired after pretreatment with pertussis toxin. These results indicate that the myocyte alpha-1 adrenergic receptor is coupled to a polyphosphoinositide-specific phospholipase C by a pertussis toxin insensitive G protein and suggest that under certain conditions IP3 may serve an important role in alpha-1 adrenergic modulation of cardiac function.
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PMID:Alpha-1 adrenergic stimulation of 1,4,5-inositol trisphosphate formation in ventricular myocytes. 255 Jun 17

Stimulation-induced noradrenaline (NA) release in rabbit hippocampus is inhibited by activation of presynaptic alpha 2-adrenoceptors and kappa-opioid receptors. The purpose of the present study was to investigate (a) an interference between the alpha 2- and kappa-mechanisms, and (b) a coupling of the opioid receptors to pertussis toxin (PT)-sensitive guanine nucleotide-binding proteins (G proteins), as has been previously shown for the alpha 2-receptors. [3H]NA release from hippocampal slices was evoked by electrical field stimulation (360 pulses/3 Hz). Inhibition of stimulation-evoked NA release by the preferential kappa-receptor agonist ethylketocyclazocine (EKC) was increased in the presence of the alpha 2-adrenoceptor antagonist yohimbine (0.1 or 1.0 microM). When autoinhibition was completely removed, EKC (1 microM) almost abolished transmitter release. Pretreatment of hippocampal tissue with either PT (8 micrograms/ml; 18 h) or N-ethylmaleimide (NEM) (30 microM; 30 min), which has been shown to alkylate PT substrates, diminished the EKC-produced inhibition of NA release. The kappa-mechanism was still impaired by these compounds when the alpha 2-receptors were blocked with yohimbine. An effect of NEM on the active site of the kappa-receptor seems to be unlikely, because NEM diminished the EKC-induced inhibition of release irrespective of whether or not the opioid receptor was occupied by EKC during exposure to NEM. The present results suggest an interference of both alpha 2- and kappa-opioid receptor-coupled signal transduction possibly through competition for a common pool of G proteins.
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PMID:Presynaptic kappa-opioid receptors on noradrenergic nerve terminals couple to G proteins and interact with the alpha 2-adrenoceptors. 255 17

The voltage-dependent calcium current in chemically differentiated NG108-15 cells is depressed by noradrenaline acting on alpha-adrenoreceptors. The response is absent in cells pretreated with pertussis toxin, implicating the involvement of a G-protein. To identify this G-protein, we have studied the response to noradrenaline in cells preinjected with antibodies specific for two G-proteins, Gi and Go. Cells injected with the Gi antibody responded normally to noradrenaline. In contrast, the response to noradrenaline in cells injected with the Go antibody was markedly attenuated. We conclude that Go is employed in coupling alpha-adrenoreceptors to the calcium channels in NG108-15 cells.
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PMID:Antibodies to the GTP binding protein, Go, antagonize noradrenaline-induced calcium current inhibition in NG108-15 hybrid cells. 256 Mar 91

Two cell cultures, NEP2 and NEM2, isolated from human foetal brain have been maintained through several passages and found to express some properties of astrocytes. Both cell cultures contain adenylate cyclase stimulated by catecholamines with a potency order of isoprenaline greater than adrenaline greater than salbutamol much greater than noradrenaline, which is consistent with the presence of beta 2-adrenergic receptors. This study reports that the beta 2-adrenergic-selective antagonist ICI 118,551 is approximately 1,000 times more potent at inhibiting isoprenaline stimulation of cyclic AMP (cAMP) formation in both NEP2 and NEM2 than the beta 1-adrenergic-selective antagonist practolol. This observation confirms the presence of beta 2-adrenergic receptors in these cell cultures. The formation of cAMP in NEP2 is also stimulated by 5'-(N-ethylcarboxamido)adenosine (NECA) more potently than by either adenosine or N6-(L-phenylisopropyl)adenosine (L-PIA), which suggests that this foetal astrocyte expresses adenosine A2 receptors. Furthermore, L-PIA and NECA inhibit isoprenaline stimulation of cAMP formation, a result suggesting the presence of adenosine A1 receptors on NEP2. The presence of A1 receptors is confirmed by the observation that the A1-selective antagonist 8-cyclopentyl-1,3-dipropylxanthine reverses the inhibition of isoprenaline stimulation of cAMP formation by L-PIA and NECA. Additional evidence that NEP2 expresses adenosine receptors linked to the adenylate cyclase-inhibitory GTP-binding protein is provided by the finding that pretreatment of these cells with pertussis toxin reverses the adenosine inhibition of cAMP formation stimulated by either isoprenaline or forskolin.
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PMID:Regulation of cyclic AMP formation in cultures of human foetal astrocytes by beta 2-adrenergic and adenosine receptors. 256 6


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