The histamine H<sub>1</sub> receptor in GT1‐7 neuronal cells is regulated by calcium influx and KN‐62, a putative inhibitor of calcium/calmodulin protein kinase II

Zamani, Melika; Bristow, David R.

doi:10.1111/j.1476-5381.1996.tb15514.x

Cited by 19 publications

(13 citation statements)

References 37 publications

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“…The Ca 2+ /calmodulin‐dependent protein kinase (CaMK) has been implicated in the homologous desensitization of histamine H 1 ‐receptors in the GT1–7 neuronal cell line (Zamani & Bristow, 1996). In HEPES buffer to which no Ca 2+ had been added, a 20 min pretreatment with 10 μ m KN‐62, a selective CaMK inhibitor did not alter the initial peak increase in [Ca 2+ ] i stimulated by 100 μ m histamine (4 ± 8% decrease in the presence of KN‐62, n = 4) (Figure 7c).…”

Section: Resultsmentioning

confidence: 99%

Dual effects of histamine and substance P on intracellular calcium levels in human U373 MG astrocytoma cells: role of protein kinase C

Young

Pinnock

Gibson

et al. 1998

British J Pharmacology

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1 In human U373 MG astrocytoma cells agonist-induced increases in intracellular Ca 2+ ([Ca 2+ ] i ) are rapidly returned towards prestimulated levels. Examination of the e ect of histamine and substance P on [Ca 2+ ] i in thapsigargin-treated cells has allowed a mechanism contributing to this e ect to be characterized. 4 Treatment of U373 MG cells with 5 mM thapsigargin, followed by the readdition of 1.8 mM Ca 2+ to the perfusion bu er, resulted in a steady-state level of [Ca 2+ ] i 97+5 nM above pretreated levels (measured 400 s after readdition of Ca 2+ ). Perfusion of histamine (100 mM, 100 s) caused a rapid decline in the thapsigargin-induced steady state level of [Ca 2+ ] i . This e ect of histamine was normally reversible upon washout. The best-®t EC 50 for the histamine response was 0.8+0.2 mM. Substance P (10 nM, 100 s) also caused a reduction in thapsigargin-induced steady-state levels of [Ca 2+ ] i . 5 Neither 100 mM histamine nor 10 nM substance P inhibited the rate of quench of fura-2¯uorescence by Mn 2+ in U373 MG cells pretreated with 5 mM thapsigargin, indicating that the depressant e ect on steady-state raised [Ca 2+ ] i was probably not due to a block of Ca 2+ entry. 6 The depressant e ect of histamine on [Ca 2+ ] i was blocked by 1 mM mepyramine, and was partially reduced by pre-incubation with 1 mM staurosporine (61+7% reduction) and with Ro 31-8220 (24+10% and 50+6% reduction by 1 and 10 mM Ro 31-8220, respectively). Pre-incubation with H-89 did not alter the depressant e ect of histamine. 7 Neither 1 mM staurosporine nor 10 mM KN-62 inhibited the binding of [ 3 H]-mepyramine to guineapig cerebellar membranes, whereas it was reduced by 17+1% and 55+2% by 1 and 10 mM Ro 31-8220, respectively. However, [ 3 H]-IP 1 accumulation stimulated by histamine in U373 MG cells was not inhibited by 1 or 10 mM Ro 31-8220 and in 2 out of 3 experiments there was a signi®cant potentiation of the response to histamine with both concentrations of Ro 31-8220. Staurosporine, 1 mM, similarly potentiated the response to 100 mM histamine in 3 out of 4 experiments. KN-62 (10 mM) did not stimulate histamine-induced [ 3 H]-IP 1 accumulation. 8 In HEPES bu er to which no Ca 2+ had been added, histamine stimulated a transient 451+107 nM increase in [Ca 2+ ] i . Pretreatment with 1 mM and 10 mM Ro 31-8220 did not signi®cantly alter the initial peak response to histamine, but slowed the rate at which histamine-induced increases in [Ca 2+ ] i were returned to prestimulated levels. Pretreatment with KN-62 had no signi®cant e ect on the response to histamine, but consistently inhibited the secondary slower phase of the decline in [Ca 2+ ] i . H-89 did not alter the histamine response. 9 The e ect of histamine in stimulating Ca 2+ extrusion was not con®ned to U373 MG cells, since 100 mM histamine also caused a rapid decrease in steady-state levels of [Ca 2+ ] i in thapsigargin-treated human HeLa cells. 10 The results indicate that agonists which increase [Ca 2+ ] i via activation of phosphoinositide metabolism can also...

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Section: Resultsmentioning

confidence: 99%

Dual effects of histamine and substance P on intracellular calcium levels in human U373 MG astrocytoma cells: role of protein kinase C

Young

Pinnock

Gibson

et al. 1998

British J Pharmacology

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“…Uncoupling of the receptor as a result of phosphorylation by protein kinases is often involved in desensitization of G-protein-coupled receptors (20), which, with regard to the H 1 R, has so far been demonstrated following activation of protein kinase C, protein kinase A, calcium/calmodulin protein kinase II, and a putative H 1 R-specific kinase (21)(22)(23)(24). In the present study, there is evidence to suggest that activation of PKA is likely to be involved in H 1 R desensitization, as an inhibitor of PKA, H-89, completely blocked the IL-1␤-induced reduction in IP formation by histamine.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of Interleukin 1 β -Induced Human Airway Smooth Muscle Hyporesponsiveness to Histamine

Pype

Xu²,

Schuermans³

et al. 2001

Am J Respir Crit Care Med

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We have investigated the effect of IL-1beta on histamine H(1)-receptor (H(1)R)-mediated inositol phosphate (IP) accumulation in human airway smooth muscle cells (HASMC) and on histamine-induced contraction of human bronchial rings. Stimulation of HASMC for 24 h with IL-1beta resulted in significant loss of histamine-induced IP formation, which was associated with a reduction of histamine- induced contraction of IL-1beta-treated human bronchial rings. An inhibitor of NF-kappaB activation, pyrrolidine dithiocarbamate, and a p38 MAPK inhibitor, blocked the IL-1beta-induced H(1)R desensitization, whereas anisomycin, an SAPK/JNK and p38 MAPK activator, mimicked the effect of IL-1beta. IL-1beta has been demonstrated to induce cox-2 expression and PGE(2) synthesis. In our study, indomethacin a cox antagonist, completely inhibited the effect of IL-1beta on H(1)R, whereas exogenously added PGE(2) was able to desensitize H(1)R. Furthermore, H-89, a selective PKA inhibitor, antagonized the effect of IL-1beta. Here, we have demonstrated that IL-1beta desensitizes H(1)R, which involves the activation of p38 MAPK and NF-kappaB, leading to the expression of cox-2 and the synthesis of PGE(2). PGE(2) increases intracellular cAMP resulting in PKA activation, which phosphorylates and functionally uncouples H(1)R. Our results suggest that IL-1beta protects airway smooth muscle against histamine-induced contractile responses and that bronchial hyperreactivity to histamine is not associated with proinflammatory cytokine-induced enhancement in H(1)R signaling.

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“…Intracellular Ca>~levels were imaged as previously described (Zamani and Bristow, 1996). During cell stimulation, images were captured at 2-s intervals.…”

Section: Measurement Of [Ca2 ÷ Lmentioning

confidence: 99%

Identification of Kainate Receptor‐Mediated Intracellular Calcium Increases in Cultured Rat Cerebellar Granule Cells

Savidge

Bleakman²,

Bristow

1997

Journal of Neurochemistry

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Abstract:The functional expression of the kainate subtype of glutamate receptor (GIuR) has been investigated in cultured rat cerebellar granule cells using single cell intracellular calcium ([Ca 2~J 1) Neurochem. 69, 1763Neurochem. 69, -1766Neurochem. 69, (1997.Glutamate, the principal excitatory neurotransmitter in the CNS, acts on three major types of ionotropic receptor: NMDA, a-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA), and kainate (Collingridge and Lester, 1989). Expression cloning has revealed four AMPA receptor subunits GluRl-4, which can all form functional channels (Hollman and Heinemann, 1994). Cloned kainate receptor subunits consist of G1uR5-7 and the high-affinity kainatebinding proteins KAi and KA2. Of the kainate receptor subunits, only GluR5 and G1uR6 appear to form functional homomeric receptors (Fletcher and Lodge, 1996).Kainate acts as a nondesensitising agonist at AMPA receptors, but as a rapidly desensitising agonist at kainate receptors. AMPA, which acts as a rapidly desensitising agonist at AMPA receptors, activates certain kainate receptors, generally producing a nondesensitising response (Fletcher and Lodge, 1996). Studies of recombinant AMPA and kainate receptors have revealed that their desensitisation can be selectively modified by cyclothiazide (CYZ) and concanavalin A (Con A), respectively (Partin et al., 1993). Desensitisation at AMPA receptors is blocked by CYZ, but only weakly attenuated by Con A. Kainate receptor desensitisation is blocked irreversibly by incubation with Con A, but unaffected by CYZ. Similar conclusions are drawn from experiments on dorsal root ganglion (DRG) neurons, which appear to express predominantly G1uR5 kaïnate receptor subunit mRNA and show responses to kainate that are potentiated by Con A, but not CYZ (Wong and Mayer, 1993).Functional discrimination between native AMPA and kainate receptors has proved difficult because of the lack of selective agonists and antagonists for the two receptor types.Native kainate receptors, which respond to kainate with a rapidly desensitising inward current, have been identified in a subset of hippocampal neurons lacking AMPA receptors (Lerma et al., 1993). However, as most cells express both AMPA and kainate receptor subunits (Fletcher and Lodge, 1996), the nondesensitising actions of kainate at AMPA receptors have made it difficult to detect rapidly desensitising responses of kainate acting at kainate receptors. Recently, a number of studies with a class of 2,3-benzodiazepines have indicated that these compounds show selectivity for AMPA receptors over kainate receptors (for review, see Vizi et al., 1996). Of these, LY300168 (formerly GYK153655) has been shown in hippocampal neurons to be a selective noncompetitive antagonist at AMPA receptors, with little activity at kainate receptors (Paternain et al., 1995). Bleakman et al. (1 996a) further characterised the potency and specificity of LY300 168 for AMPA receptors over kainate receptors at recombinant AMPA and kainate receptors and native receptor...

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The histamine H₁ receptor in GT1‐7 neuronal cells is regulated by calcium influx and KN‐62, a putative inhibitor of calcium/calmodulin protein kinase II

Cited by 19 publications

References 37 publications

Dual effects of histamine and substance P on intracellular calcium levels in human U373 MG astrocytoma cells: role of protein kinase C

Dual effects of histamine and substance P on intracellular calcium levels in human U373 MG astrocytoma cells: role of protein kinase C

Mechanisms of Interleukin 1 β -Induced Human Airway Smooth Muscle Hyporesponsiveness to Histamine

Identification of Kainate Receptor‐Mediated Intracellular Calcium Increases in Cultured Rat Cerebellar Granule Cells

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The histamine H1 receptor in GT1‐7 neuronal cells is regulated by calcium influx and KN‐62, a putative inhibitor of calcium/calmodulin protein kinase II

Cited by 19 publications

References 37 publications

Dual effects of histamine and substance P on intracellular calcium levels in human U373 MG astrocytoma cells: role of protein kinase C

Dual effects of histamine and substance P on intracellular calcium levels in human U373 MG astrocytoma cells: role of protein kinase C

Mechanisms of Interleukin 1 β -Induced Human Airway Smooth Muscle Hyporesponsiveness to Histamine

Identification of Kainate Receptor‐Mediated Intracellular Calcium Increases in Cultured Rat Cerebellar Granule Cells

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The histamine H₁ receptor in GT1‐7 neuronal cells is regulated by calcium influx and KN‐62, a putative inhibitor of calcium/calmodulin protein kinase II