2023 |
Walweel K, Beard N, van Helden DF, Laver DR, 'Dantrolene inhibition of ryanodine channels (RyR2) in artificial lipid bilayers depends on FKBP12.6.', J Gen Physiol, 155 (2023) [C1]
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Nova |
2022 |
Tamanna S, Morosin SK, Delforce SJ, van Helden DF, Lumbers ER, Pringle KG, 'Renin-angiotensin system (RAS) enzymes and placental trophoblast syncytialisation', MOLECULAR AND CELLULAR ENDOCRINOLOGY, 547 (2022) [C1]
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Nova |
2022 |
van Helden DF, 'Insights into permeability control of the fenestrated endothelium of the jejunal microvasculature', PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 474 485-486 (2022)
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2021 |
Tamanna S, Clifton VL, Rae K, van Helden DF, Lumbers ER, Pringle KG, 'Angiotensin Converting Enzyme 2 (ACE2) in Pregnancy: Preeclampsia and Small for Gestational Age (vol 11, 590787, 2020)', FRONTIERS IN PHYSIOLOGY, 12 (2021)
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2021 |
Mitsui R, Hashitani H, Lang RJ, van Helden DF, 'Mechanisms underlying spontaneous phasic contractions and sympathetic control of smooth muscle in the rat caudal epididymis', PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 473 1925-1938 (2021) [C1]
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Nova |
2021 |
Ferdoushi A, Griffin N, Marsland M, Xu X, Faulkner S, Gao F, et al., 'Tumor innervation and clinical outcome in pancreatic cancer', SCIENTIFIC REPORTS, 11 (2021) [C1]
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Nova |
2021 |
Pineda S, Nikolova-Krstevski V, Leimena C, Atkinson AJ, Altekoester AK, Cox CD, et al., 'Conserved Role of the Large Conductance Calcium-Activated Potassium Channel, K
Background: KCNMA1 encodes the a-subunit of the large-conductance Ca2+-activated K+ channel, KCa1.1, and lies within a linkage interval for atrial fibrillation (AF). Insights into... [more]
Background: KCNMA1 encodes the a-subunit of the large-conductance Ca2+-activated K+ channel, KCa1.1, and lies within a linkage interval for atrial fibrillation (AF). Insights into the cardiac functions of KCa1.1 are limited, and KCNMA1 has not been investigated as an AF candidate gene. Methods: The KCNMA1 gene was sequenced in 118 patients with familial AF. The role of KCa1.1 in normal cardiac structure and function was evaluated in humans, mice, zebrafish, and fly. A novel KCNMA1 variant was functionally characterized. Results: A complex KCNMA1 variant was identified in 1 kindred with AF. To evaluate potential disease mechanisms, we first evaluated the distribution of KCa1.1 in normal hearts using immunostaining and immunogold electron microscopy. KCa1.1 was seen throughout the atria and ventricles in humans and mice, with strong expression in the sinus node. In an ex vivo murine sinoatrial node preparation, addition of the KCa1.1 antagonist, paxilline, blunted the increase in beating rate induced by adrenergic receptor stimulation. Knockdown of the KCa1.1 ortholog, kcnma1b, in zebrafish embryos resulted in sinus bradycardia with dilatation and reduced contraction of the atrium and ventricle. Genetic inactivation of the Drosophila KCa1.1 ortholog, slo, systemically or in adult stages, also slowed the heartbeat and produced fibrillatory cardiac contractions. Electrophysiological characterization of slo-deficient flies revealed bursts of action potentials, reflecting increased events of fibrillatory arrhythmias. Flies with cardiac-specific overexpression of the human KCNMA1 mutant also showed increased heart period and bursts of action potentials, similar to the KCa1.1 loss-of-function models. Conclusions: Our data point to a highly conserved role of KCa1.1 in sinus node function in humans, mice, zebrafish, and fly and suggest that KCa1.1 loss of function may predispose to AF.
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Nova |
2020 |
Ferdoushi A, Li X, Griffin N, Faulkner S, Jamaluddin MFB, Gao F, et al., 'Schwann Cell Stimulation of Pancreatic Cancer Cells: A Proteomic Analysis', Frontiers in Oncology, 10 (2020) [C1]
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Nova |
2020 |
Lee JM, Mayall JR, Chevalier A, McCarthy H, Van Helden D, Hansbro PM, et al., 'Chlamydia muridarum infection differentially alters smooth muscle function in mouse uterine horn and cervix', American Journal of Physiology - Endocrinology and Metabolism, 318 E981-E994 (2020) [C1]
Lee JM, Mayall JR, Chevalier A, McCarthy H, Van Helden D, Hansbro PM, Horvat JC, Jobling P. Chlamydia muridarum infection differentially alters smooth muscle function in mouse ute... [more]
Lee JM, Mayall JR, Chevalier A, McCarthy H, Van Helden D, Hansbro PM, Horvat JC, Jobling P. Chlamydia muridarum infection differentially alters smooth muscle function in mouse uterine horn and cervix. Am J Physiol Endocrinol Metab 318: E981 E994, 2020. First published April 21, 2020; doi:10.1152/ajpendo.00513. 2019. Chlamydia trachomatis infection is a primary cause of reproductive tract diseases including infertility. Previous studies showed that this infection alters physiological activities in mouse oviducts. Whether this occurs in the uterus and cervix has never been investigated. This study characterized the physiological activities of the uterine horn and the cervix in a Chlamydia muridarum (Cmu)-infected mouse model at three infection time points of 7, 14, and 21 days postinfection (dpi). Cmu infection significantly decreased contractile force of spontaneous contraction in the cervix (7 and 14 dpi; P < 0.001 and P < 0.05, respectively), but this effect was not observed in the uterine horn. The responses of the uterine horn and cervix to oxytocin were significantly altered by Cmu infection at 7 dpi (P < 0.0001), but such responses were attenuated at 14 and 21 dpi. Cmu infection increased contractile force to prostaglandin (PGF2_) by 53 83% in the uterine horn. This corresponded with the increased messenger ribonucleic acid (mRNA) expression of Ptgfr that encodes for its receptor. However, Cmu infection did not affect contractions of the uterine horn and cervix to PGE2 and histamine. The mRNA expression of Otr and Ptger4 was inversely correlated with the mRNA expression of Il1b, Il6 in the uterine horn of Cmu-inoculated mice (P < 0.01 to P < 0.001), suggesting that the changes in the Otr and Ptger4 mRNA expression might be linked to the changes in inflammatory cytokines. Lastly, this study also showed a novel physiological finding of the differential response to PGE2 in mouse uterine horn and cervix.
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Nova |
2020 |
Ashna A, van Helden DF, Dos Remedios C, Molenaar P, Laver DR, 'Phenytoin Reduces Activity of Cardiac Ryanodine Receptor 2; A Potential Mechanism for Its Cardioprotective Action.', Mol Pharmacol, 97 250-258 (2020) [C1]
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Nova |
2020 |
Tamanna S, Clifton VL, Rae K, van Helden DF, Lumbers ER, Pringle KG, 'Angiotensin Converting Enzyme 2 (ACE2) in Pregnancy: Preeclampsia and Small for Gestational Age', Frontiers in Physiology, 11 1-10 (2020) [C1]
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Nova |
2019 |
de Oliveira RB, Petiz LL, Lim R, Lipski J, Gravina FS, Brichta AM, et al., 'Crosstalk between mitochondria, calcium channels and actin cytoskeleton modulates noradrenergic activity of locus coeruleus neurons.', Journal of neurochemistry, 149 471-487 (2019) [C1]
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Nova |
2019 |
Walweel K, Gomez-Hurtado N, Rebbeck RT, Oo YW, Beard NA, Molenaar P, et al., 'Calmodulin inhibition of human RyR2 channels requires phosphorylation of RyR2-S2808 or RyR2-S2814', Journal of Molecular and Cellular Cardiology, 130 96-106 (2019) [C1]
Calmodulin (CaM) is a Ca-binding protein that binds to, and can directly inhibit cardiac ryanodine receptor calcium release channels (RyR2). Animal studies have shown that RyR2 hy... [more]
Calmodulin (CaM) is a Ca-binding protein that binds to, and can directly inhibit cardiac ryanodine receptor calcium release channels (RyR2). Animal studies have shown that RyR2 hyperphosphorylation reduces CaM binding to RyR2 in failing hearts, but data are lacking on how CaM regulates human RyR2 and how this regulation is affected by RyR2 phosphorylation. Physiological concentrations of CaM (100 nM) inhibited the diastolic activity of RyR2 isolated from failing human hearts by ~50% but had no effect on RyR2 from healthy human hearts. Using FRET between donor-FKBP12.6 and acceptor-CaM bound to RyR2, we determined that CaM binds to RyR2 from healthy human heart with a K d = 121 ± 14 nM. Ex-vivo phosphorylation/dephosphorylation experiments suggested that the divergent CaM regulation of healthy and failing human RyR2 was caused by differences in RyR2 phosphorylation by protein kinase A and Ca-CaM-dependent kinase II. Ca 2+ -spark measurements in murine cardiomyocytes harbouring RyR2 phosphomimetic or phosphoablated mutants at S2814 and S2808 suggest that phosphorylation of residues corresponding to either human RyR2-S2808 or S2814 is both necessary and sufficient for RyR2 regulation by CaM. Our results challenge the current concept that CaM universally functions as a canonical inhibitor of RyR2 across species. Rather, CaM's biological action on human RyR2 appears to be more nuanced, with inhibitory activity only on phosphorylated RyR2 channels, which occurs during exercise or in patients with heart failure.
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Nova |
2019 |
van Heiden DF, Dosen PJ, O'Leary MA, Isbister GK, 'Two pathways for venom toxin entry consequent to injection of an Australian elapid snake venom', SCIENTIFIC REPORTS, 9 (2019) [C1]
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Nova |
2018 |
Donovan LC, Douglas CD, Van Helden D, 'Wound tension and 'closability' with keystone flaps, V-Y flaps and primary closure: a study in fresh-frozen cadavers.', Widespread white matter microstructural differences in schizophrenia across 4322 individuals: results from the ENIGMA Schizophrenia DTI Working Group., 88 486-490 (2018) [C1]
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Nova |
2018 |
Donovan LC, Douglas CD, Van Helden D, 'Response to Re: Wound tension and 'closability' with keystone flaps, V-Y flaps and primary closure: a study in fresh-frozen cadavers', ANZ JOURNAL OF SURGERY, 88 1089-1089 (2018)
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2017 |
van Helden DF, Kamiya A, Kelsey S, Laver DR, Jobling P, Mitsui R, Hashitani H, 'Nerve-induced responses of mouse vaginal smooth muscle', Pflugers Archiv European Journal of Physiology, 469 1373-1385 (2017) [C1]
Neural and agonist-induced contractions of proximal (i.e. upper half adjacent to the cervix) and distal mouse vaginal smooth muscle strips were investigated. We hypothesised that ... [more]
Neural and agonist-induced contractions of proximal (i.e. upper half adjacent to the cervix) and distal mouse vaginal smooth muscle strips were investigated. We hypothesised that nerve-mediated vaginal contractions arise through activity of cholinergic nerves. Nerve activation by bursts of electrical field stimulation (EFS) caused a primary transient contraction often accompanied by a secondary transient contraction, both larger in proximal than distal tissues (i.e. primary: 7-fold larger; secondary: 3-fold larger). Our hypothesis was supported as we found that cholinergic nerves mediated the primary transient contraction in both proximal and distal vaginal strips, as EFS responses were enhanced by neostigmine an anticholinesterase, massively inhibited by the competitive muscarinic receptor antagonist atropine and not affected by the non-selective a-adrenergic receptor antagonist phentolamine. Primary transient contractions were halved in amplitude by the L-type Ca2+ channel blocker nifedipine and markedly inhibited by the sarco-endoplasmic reticulum calcium ATPase (SERCA) inhibitor cyclopiazonic acid (CPA). Resultant secondary transient contractions were abolished by nifedipine. Notably, the selective a1-adrenergic receptor agonist phenylephrine caused tonic contracture in distal but not proximal strips. Low-frequency EFS often initiated recurrent transient contractions similar to those elicited by CCh. Immunohistochemical studies demonstrated innervation of the smooth muscle. Findings of enhanced proximal cholinergic nerve-induced transient contractions, evidence that maintained nerve stimulation could cause recurrent contractions and the finding of distal phenylephrine-mediated tonic contraction have implications on insemination.
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Nova |
2017 |
Dora KA, van Helden DF, 'Endothelial tubes: another window into lymphatic function', JOURNAL OF PHYSIOLOGY-LONDON, 595 7267-7268 (2017)
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2017 |
Walweel K, Gomez-Hurtado N, Oo YW, Beard NA, dos Remedios C, Johnson CN, et al., 'Calmodulin Mutants Linked to Catecholaminergic Polymorphic Ventricular Tachycardia Fail to Inhibit Human RyR2 Channels', JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 70 115-117 (2017)
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2017 |
Walweel K, Molenaar P, Imtiaz MS, Denniss A, dos Remedios C, van Helden DF, et al., 'Ryanodine receptor modification and regulation by intracellular Ca
Rationale Heart failure is a multimodal disorder, of which disrupted Ca2¿+ homeostasis is a hallmark. Central to Ca2¿+ homeostasis is the major cardiac Ca2¿+ release channel ¿ the... [more]
Rationale Heart failure is a multimodal disorder, of which disrupted Ca2¿+ homeostasis is a hallmark. Central to Ca2¿+ homeostasis is the major cardiac Ca2¿+ release channel ¿ the ryanodine receptor (RyR2) ¿ whose activity is influenced by associated proteins, covalent modification and by Ca2¿+ and Mg2¿+. That RyR2 is remodelled and its function disturbed in heart failure is well recognized, but poorly understood. Objective To assess Ca2¿+ and Mg2¿+ regulation of RyR2 from left ventricles of healthy, cystic fibrosis and failing hearts, and to correlate these functional changes with RyR2 modifications and remodelling. Methods and results The function of RyR2 from left ventricular samples was assessed using lipid bilayer single-channel measurements, whilst RyR2 modification and protein:protein interactions were determined using Western Blots and co-immunoprecipitation. In all failing hearts there was an increase in RyR2 activity at end-diastolic cytoplasmic Ca2¿+ (100¿nM), a decreased cytoplasmic [Ca2¿+] required for half maximal activation (Ka) and a decrease in inhibition by cytoplasmic Mg2¿+. This was accompanied by significant hyperphosphorylation of RyR2 S2808 and S2814, reduced free thiol content and a reduced interaction with FKBP12.0 and FKBP12.6. Either dephosphorylation of RyR2 using PP1 or thiol reduction using DTT eliminated any significant difference in the activity of RyR2 from healthy and failing hearts. We also report a subgroup of RyR2 in failing hearts that were not responsive to regulation by intracellular Ca2¿+ or Mg2¿+. Conclusion Despite different aetiologies, disrupted RyR2 Ca2¿+ sensitivity and biochemical modification of the channel are common constituents of failing heart RyR2 and may underlie the pathological disturbances in intracellular Ca2¿+ signalling.
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Nova |
2017 |
Carreiro JN, Magnani M, Jobling P, van Helden DF, Nalivaiko E, Braga VA, 'Resveratrol restores uterine contractions during hypoxia by blockade of ATP-sensitive potassium channels', Journal of Functional Foods, 33 307-313 (2017) [C1]
This study assessed the¿effects of resveratrol, a polyphenol¿found in grapes and red wine¿on non-pregnant murine uteri under hypoxia. Resveratrol at 1, 3, 10, 30 and 100¿µM promot... [more]
This study assessed the¿effects of resveratrol, a polyphenol¿found in grapes and red wine¿on non-pregnant murine uteri under hypoxia. Resveratrol at 1, 3, 10, 30 and 100¿µM promoted uterine relaxation and decreased the amplitude and frequency of spontaneous uterine contractions. Assayed at 3, 10, 30¿µM, resveratrol inhibited the oxytocin-induced cumulative contractions reducing the maximum effect in a dose-dependent manner. In hypoxic uteri, resveratrol at 100¿µM restored the uterine contractions compromised by hypoxia. In addition, under hypoxia, resveratrol prevented the decrease in uterine contractions maintaining >75% of its contraction capability. The effects of resveratrol on uterine contractions under hypoxia were attenuated by tetraethylammonium (10¿mM) and almost abolished by glibenclamide (10¿µM). Our¿results show regenerative and protective effects of resveratrol in non-pregnant murine uteri under hypoxia and describes for the first time that these effects are mediated by blockade of ATP-sensitive potassium channels.
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Nova |
2015 |
Zhang HM, Van Helden DF, McCurdy DW, Offler CE, Patrick JW, 'Plasma Membrane Ca
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Nova |
2015 |
Zhang HM, Imtiaz MS, Laver DR, McCurdy DW, Offler CE, Van Helden DF, Patrick JW, 'Polarized and persistent Ca
Transfer cell morphology is characterized by a polarized ingrowth wall comprising a uniform wall upon which wall ingrowth papillae develop at right angles into the cytoplasm. The ... [more]
Transfer cell morphology is characterized by a polarized ingrowth wall comprising a uniform wall upon which wall ingrowth papillae develop at right angles into the cytoplasm. The hypothesis that positional information directing construction of wall ingrowth papillae is mediated by Ca2+ signals generated by spatiotemporal alterations in cytosolic Ca2+ ([Ca2+]cyt) of cells trans-differentiating to a transfer cell morphology was tested. This hypothesis was examined using Vicia faba cotyledons. On transferring cotyledons to culture, their adaxial epidermal cells synchronously trans-differentiate to epidermal transfer cells. A polarized and persistent Ca2+ signal, generated during epidermal cell trans-differentiation, was found to co-localize with the site of ingrowth wall formation. Dampening Ca2+ signal intensity, by withdrawing extracellular Ca2+ or blocking Ca2+ channel activity, inhibited formation of wall ingrowth papillae. Maintenance of Ca2+ signal polarity and persistence depended upon a rapid turnover (minutes) of cytosolic Ca2+ by co-operative functioning of plasma membrane Ca2+-permeable channels and Ca2+-ATPases. Viewed paradermally, and proximal to the cytosol-plasma membrane interface, the Ca2+ signal was organized into discrete patches that aligned spatially with clusters of Ca2+-permeable channels. Mathematical modelling demonstrated that these patches of cytosolic Ca2+ were consistent with inward-directed plumes of elevated [Ca2+]cyt. Plume formation depended upon an alternating distribution of Ca2+-permeable channels and Ca2+-ATPase clusters. On further inward diffusion, the Ca2+ plumes coalesced into a uniform Ca2+ signal. Blocking or dispersing the Ca2+ plumes inhibited deposition of wall ingrowth papillae, while uniform wall formation remained unaltered. A working model envisages that cytosolic Ca2+ plumes define the loci at which wall ingrowth papillae are deposited.
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Nova |
2015 |
Nikolaev YA, Dosen PJ, Laver DR, Van Helden DF, Hamill OP, 'Single mechanically-gated cation channel currents can trigger action potentials in neocortical and hippocampal pyramidal neurons', Brain Research, 1608 1-13 (2015) [C1]
The mammalian brain is a mechanosensitive organ that responds to different mechanical forces ranging from intrinsic forces implicated in brain morphogenesis to extrinsic forces th... [more]
The mammalian brain is a mechanosensitive organ that responds to different mechanical forces ranging from intrinsic forces implicated in brain morphogenesis to extrinsic forces that can cause concussion and traumatic brain injury. However, little is known of the mechanosensors that transduce these forces. In this study we use cell-attached patch recording to measure single mechanically-gated (MG) channel currents and their affects on spike activity in identified neurons in neonatal mouse brain slices. We demonstrate that both neocortical and hippocampal pyramidal neurons express stretch-activated MG cation channels that are activated by suctions of ~25 mm Hg, have a single channel conductance for inward current of 50-70 pS and show weak selectivity for alkali metal cations (i.e., Na+<K+<Cs+). Significantly, single MG channel currents activated on the soma trigger spiking/action potentials in both neocortical and hippocampal pyramidal neurons. Not all neuron types studied here expressed MG channel currents. In particular, locus coeruleus and cerebellar Purkinje neurons showed no detectable MG channel activity. Moreover their robust rhythmic spike activity was resistant to mechanical modulation. Our observation that a single MG channel current can trigger spiking predicates the need for reassessment of the long held view that the impulse output of central neurons depends only upon their intrinsic voltage-gated channels and/or their integrated synaptic input.
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Nova |
2015 |
Beard DJ, Mcleod DD, Logan CL, Murtha LA, Imtiaz MS, Van Helden DF, Spratt NJ, 'Intracranial pressure elevation reduces flow through collateral vessels and the penetrating arterioles they supply. A possible explanation for 'collateral failure' and infarct expansion after ischemic stroke', Journal of Cerebral Blood Flow and Metabolism, 35 861-872 (2015) [C1]
Recent human imaging studies indicate that reduced blood flow through pial collateral vessels ('collateral failure') is associated with late infarct expansion despite st... [more]
Recent human imaging studies indicate that reduced blood flow through pial collateral vessels ('collateral failure') is associated with late infarct expansion despite stable arterial occlusion. The cause for 'collateral failure' is unknown. We recently showed that intracranial pressure (ICP) rises dramatically but transiently 24 hours after even minor experimental stroke. We hypothesized that ICP elevation would reduce collateral blood flow. First, we investigated the regulation of flow through collateral vessels and the penetrating arterioles arising from them during stroke reperfusion. Wistar rats were subjected to intraluminal middle cerebral artery (MCA) occlusion (MCAo). Individual pial collateral and associated penetrating arteriole blood flow was quantified using fluorescent microspheres. Baseline bidirectional flow changed to MCA-directed flow and increased by >450% immediately after MCAo. Collateral diameter changed minimally. Second, we determined the effect of ICP elevation on collateral and watershed penetrating arteriole flow. Intracranial pressure was artificially raised in stepwise increments during MCAo. The ICP increase was strongly correlated with collateral and penetrating arteriole flow reductions. Changes in collateral flow post-stroke appear to be primarily driven by the pressure drop across the collateral vessel, not vessel diameter. The ICP elevation reduces cerebral perfusion pressure and collateral flow, and is the possible explanation for 'collateral failure' in stroke-in-progression.
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Nova |
2015 |
Oo YW, Gomez-Hurtado N, Walweel K, van Helden DF, Imtiaz MS, Knollmann BC, Laver DR, 'Essential Role of Calmodulin in RyR Inhibition by Dantrolene', MOLECULAR PHARMACOLOGY, 88 57-63 (2015) [C1]
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Nova |
2015 |
Hashitani H, Mitsui R, Masaki S, Van Helden DF, 'Pacemaker role of pericytes in generating synchronized spontaneous Ca2+ transients in the myenteric microvasculature of the guinea-pig gastric antrum.', Cell calcium, 58 442-456 (2015) [C1]
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Nova |
2014 |
van Helden DF, Thomas PA, Dosen PJ, Imtiaz MS, Laver DR, Isbister GK, 'Pharmacological approaches that slow lymphatic flow as a snakebite first aid.', PLoS Negl Trop Dis, 8 e2722 (2014) [C1]
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Nova |
2014 |
Walweel K, Li J, Molenaar P, Imtiaz MS, Quail A, dos Remedios CG, et al., 'Differences in the regulation of RyR2 from human, sheep, and rat by Ca² and Mg² in the cytoplasm and in the lumen of the sarcoplasmic reticulum.', J Gen Physiol, 144 263-271 (2014) [C1]
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Nova |
2014 |
Gravina FS, Van Helden DF, Kerr KP, De Oliveira RB, Jobling P, 'Phasic contractions of the mouse vagina and cervix at different phases of the estrus cycle and during late pregnancy', PLoS ONE, 9 (2014) [C1]
Conclusions/Significance: Cervical smooth muscle strips taken from mice in estrus, metestrus or late pregnancy were generally spontaneously active. Vaginal smooth muscle strips we... [more]
Conclusions/Significance: Cervical smooth muscle strips taken from mice in estrus, metestrus or late pregnancy were generally spontaneously active. Vaginal smooth muscle strips were normally quiescent but could be induced to exhibit phasic contractions independent on phase of the estrus cycle or late pregnancy. Spontaneous cervical or TEA-induced vaginal phasic contractions were not mediated by ICs or intracellular Ca2+ stores. Given that vaginal smooth muscle is normally quiescent then it is likely that increases in hormones such as oxytocin, as might occur through sexual stimulation, enhance the effectiveness of such pacemaking until phasic contractile activity emerges.
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Nova |
2014 |
Mehra D, Imtiaz MS, Van Helden DF, Knollmann BC, Laver DR, 'Multiple modes of ryanodine receptor 2 inhibition by flecainide', Molecular Pharmacology, 86 696-706 (2014) [C1]
Catecholaminergic polymorphic ventricular tachycardia (CPVT) causes sudden cardiac death due to mutations in cardiac ryanodine receptors (RyR2), calsequestrin, or calmodulin. Flec... [more]
Catecholaminergic polymorphic ventricular tachycardia (CPVT) causes sudden cardiac death due to mutations in cardiac ryanodine receptors (RyR2), calsequestrin, or calmodulin. Flecainide, a class I antiarrhythmic drug, inhibits Na<sup>+</sup> and RyR2 channels and prevents CPVT. The purpose of this study is to identify inhibitory mechanisms of flecainide on RyR2. RyR2 were isolated from sheep heart, incorporated into lipid bilayers, and investigated by singlechannel recording under various activating conditions, including the presence of cytoplasmic ATP (2mM) and a range of cytoplasmic [Ca<sup>2+</sup>], [Mg<sup>2+</sup>], pH, and [caffeine]. Flecainide applied to either the cytoplasmic or luminal sides of the membrane inhibited RyR2 by two distinct modes: 1) a fast block consisting of brief substate and closed events with a mean duration of ~1 ms, and 2) a slow block consisting of closed events with a mean duration of ~1 second. Both inhibition modes were alleviated by increasing cytoplasmic pH from 7.4 to 9.5 but were unaffected by luminal pH. The slow block was potentiated in RyR2 channels that had relatively low open probability, whereas the fast block was unaffected by RyR2 activation. These results show that these two modes are independent mechanisms for RyR2 inhibition, both having a cytoplasmic site of action. The slow mode is a closed-channel block, whereas the fast mode blocks RyR2 in the open state. At diastolic cytoplasmic [Ca<sup>2+</sup>] (100 nM), flecainide possesses an additional inhibitory mechanism that reduces RyR2 burst duration. Hence, multiple modes of action underlie RyR2 inhibition by flecainide.
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Nova |
2014 |
van Helden DF, 'The lymphangion: A not so 'primitive' heart', Journal of Physiology, 592 5353-5354 (2014) [C3]
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2013 |
Li J, Imtiaz MS, Beard NA, Dulhunty AF, Thorne R, vanHelden DF, Laver DR, 'ß-Adrenergic stimulation increases RyR2 activity via intracellular Ca2+ and Mg2+ regulation.', PLoS One, 8 e58334 (2013) [C1]
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2012 |
De Oliveira R, Gravina FS, Lim R, Brichta AM, Callister RJ, Van Helden DF, 'Heterogeneous responses to antioxidants in noradrenergic neurons of the Locus coeruleus indicate differing susceptibility to free radical content', Oxidative Medicine and Cellular Longevity, 2012 820285 (2012) [C1]
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Nova |
2011 |
De Oliveira R, Gravina FS, Lim R, Brichta AM, Callister RJ, Van Helden DF, 'Developmental changes in pacemaker currents in mouse locus coeruleus neurons', Brain Research, 1425 27-36 (2011) [C1]
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Nova |
2011 |
Laver DR, Van Helden DF, 'Three independent mechanisms contribute to tetracaine inhibition of cardiac calcium release channels', Journal of Molecular and Cellular Cardiology, 51 357-369 (2011) [C1]
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Nova |
2011 |
Saul ME, Thomas PA, Dosen PJ, Isbister GK, O'Leary MA, Whyte IM, et al., 'A pharmacological approach to first aid treatment for snakebite', Nature Medicine, 17 809-811 (2011) [C1]
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Nova |
2011 |
Gravina FS, Jobling P, Kerr KP, De Oliveira R, Parkington HC, Van Helden DF, 'Oxytocin depolarizes mitochondria in isolated myometrial cells', Experimental Physiology, 96 949-956 (2011) [C1]
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Nova |
2010 |
Sharafutdinova G, Holdsworth JL, Van Helden DF, 'Calculated two-photon fluorescence correction factors for reflective scan engines', Applied Optics, 49 1472-1479 (2010) [C1]
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Nova |
2010 |
Sharafutdinova G, Holdsworth JL, Van Helden DF, 'Improved field scanner incorporating parabolic optics. Part 2: experimental verification and potential for volume scanning', Applied Optics, 49 5517-5527 (2010) [C1]
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Nova |
2010 |
Imtiaz MS, Von Der Weid P-Y, Van Helden DF, 'Synchronization of Ca2+oscillations: A coupled oscillator-based mechanism in smooth muscle', FEBS Journal, 277 278-285 (2010) [C1]
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Nova |
2010 |
Gravina FS, Parkington HC, Kerr KP, De Oliveira R, Jobling P, Coleman HA, et al., 'Role of mitochondria in contraction and pacemaking in the mouse uterus', British Journal of Pharmacology, 161 1375-1390 (2010) [C1]
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Nova |
2010 |
Imtiaz MS, Von Der Weid P-Y, Laver DR, Van Helden DF, 'SR Ca2+ store refill-a key factor in cardiac pacemaking', Journal of Molecular and Cellular Cardiology, 49 412-426 (2010) [C1]
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Nova |
2010 |
De Oliveira R, Graham BA, Howlett MC, Gravina FS, Oliveira MW, Imtiaz MS, et al., 'Ketamine anesthesia helps preserve neuronal viability', Journal of Neuroscience Methods, 189 230-232 (2010) [C1]
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Nova |
2010 |
Van Helden DF, Laver DR, Holdsworth JL, Imtiaz MS, 'Generation and propagation of gastric slow waves', Clinical and Experimental Pharmacology and Physiology, 37 516-524 (2010) [C1]
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Nova |
2010 |
De Oliveira R, Howlett MC, Gravina FS, Imtiaz MS, Callister RJ, Brichta AM, Van Helden DF, 'Pacemaker currents in mouse locus coeruleus neurons', Neuroscience, 170 166-177 (2010) [C1]
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Nova |
2009 |
Sharafutdinova G, Holdsworth JL, Van Helden DF, 'Improved field scanner incorporating parabolic optics: Part 1: Simulation', Applied Optics, 48 4389-4396 (2009) [C1]
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Nova |
2009 |
Imtiaz MS, von der Weid P-Y, Crowe M, van Helden D, 'Lymphatic pacemaking', FASEB JOURNAL, 23 (2009) [E3] |
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2008 |
Odell AF, Van Helden DF, Scott JL, 'The spectrin cytoskeleton influences the surface expression and activation of human transient receptor potential channel 4 channels', Journal of Biological Chemistry, 283 4395-4407 (2008) [C1]
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Nova |
2008 |
Von Der Weid P-Y, Rahman M, Imtiaz MS, Van Helden DF, 'Spontaneous transient depolarizations in lymphatic vessels of the guinea pig mesentery: Pharmacology and implication for spontaneous contractility', American Journal of Physiology: Heart and Circulatory Physiology, 295 H1989-H2000 (2008) [C1]
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Nova |
2007 |
Smith R, Van Helden DF, Hirst JJ, Zakar T, Read MA, Chan EC, et al., 'Pathological interactions with the timing of birth and uterine activation', Australian & New Zealand Journal of Obstetrics & Gynaecology, 47 430-437 (2007) [C1]
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2007 |
Imtiaz MS, Zhao J, Hosaka K, Von Der Weid PY, Crowe M, Van Helden DF, 'Pacemaking through Ca2+ stores interacting as coupled oscillators via membrane depolarization', Biophysical Journal, 92 3843-3861 (2007) [C1]
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2006 |
Dielenberg R, Halasz P, Hosaka K, Van Helden DF, 'Vessel motion measurement in real-time using movement detection at multiple regions of interest', Journal of Neuroscience Methods, 152 40-47 (2006) [C1]
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2006 |
Hosaka K, Rayner SE, Von Der Weid PY, Zhao J, Imtiaz MS, Van Helden DF, 'Calcitonin gene-related peptide activates different signaling pathways in mesenteric lymphatics of guinea pigs', American Journal of Physiology-Heart and Circulatory Physiology, 290 H813-H822 (2006) [C1]
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2006 |
Van Helden DF, Hosaka K, Imtiaz MS, 'Rhythmicity in the microcirculation', Clinical Hemorheology and Microcirculation, 34 59-66 (2006) [C1]
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2006 |
Imtiaz MS, Katnik CP, Smith DW, Van Helden DF, 'Role of voltage-dependent modulation of store Ca2+ release in synchronization of Ca2+ oscillations', Biophysical Journal, 90 1-23 (2006) [C1]
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Nova |
2005 |
Odell AF, Scott JL, Van Helden DF, 'Epidermal growth factor induces tyrosine phosphorylation, membrane insertion, and activation of transient receptor potential channel 4', Journal of Biological Chemistry, 280 37974-37987 (2005) [C1]
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Nova |
2004 |
Ferrusi I, Zhao J, Van Helden DF, Von Der Weid P-Y, 'Cyclopiazonic acid decreases spontaneous transient depolarizations in guinea pig mesenteric lymphatic vessels in endothelium-dependent and -independent manners', Am J Physiol Heart Circ Physiol, 286 H2287-H2295 (2004) [C1]
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2003 |
Zhao J, Van Helden DF, 'ET-1-associated vasomotion and vasospasm in lymphatic vessels of the guinea-pig mesentery', British Journal of Pharmacology, 140 1399-1413 (2003) [C1]
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2003 |
Van Helden DF, Imtiaz MS, 'Ca2+ phase waves: a basis for cellular pacemaking and long-range synchronicity in the guinea-pig gastric pylorus', The Journal of Physiology, 548.1 271-296 (2003) [C1]
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Nova |
2002 |
Imtiaz MS, Smith DW, Van Helden DF, 'A Theoretical Model Of Slow Wave Regulation Using Voltage-Dependent Synthesis Of Inositol 1,4,5-Trisphosphate', Biophyhsical Journal, Vol. 83 1877-1890 (2002) [C1]
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2002 |
Zhao J, Van Helden DF, 'ATP-induced endothelium-independent enhancement of lymphatic vasomotion in guinea-pig mesentery involves P2x and P2y receptors', British Journal of Pharmacology, 137 477-487 (2002) [C1]
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Nova |
2001 |
Von Der Weid P-Y, Zhao J, Van Helden DF, 'Nitric oxide decreases pacemaker activity in lymphatic vessels of guinea pig mesentery', Am J Physiol Heart Circ Physiol, 280 H2707-H2716 (2001) [C1]
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2000 |
Van Helden DF, Imtiaz MS, Nurgaliyeva K, Von Der Weid P-Y, Dosen PJ, 'Role of calcium stores and membrane voltage in the generation of slow wave action potentials in guinea-pig gastric pylorus', Journal of Physiology, 524.1 245-265 (2000) [C1]
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2000 |
Van Helden D, Zhao J, 'Lymphatic Vasomotion', Clinical and Experimental Pharmacology and Physiology, 27 1014-1018 (2000) [C1]
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1999 |
Gao JN, Zhao J, Rayner SE, Van Helden DF, 'Evidence that the ATP-induced increase in vasomotion of guinea-pig mesenteric lymphatics involves an endothelium-dependent release of thromboxane A(2)', BRITISH JOURNAL OF PHARMACOLOGY, 127 1597-1602 (1999)
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1997 |
Rayner SE, VanHelden DF, 'Evidence that the substance P-induced enhancement of pacemaking in lymphatics of the guinea-pig mesentery occurs through endothelial release of thromboxane A(2)', BRITISH JOURNAL OF PHARMACOLOGY, 121 1589-1596 (1997)
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1997 |
Crowe MJ, vonderWeid PY, Brock JA, VanHelden DF, 'Co-ordination of contractile activity in guinea-pig mesenteric lymphatics', JOURNAL OF PHYSIOLOGY-LONDON, 500 235-244 (1997)
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1997 |
vonderWeid PY, VanHelden DF, 'Functional electrical properties of the endothelium in lymphatic vessels of the guinea-pig mesentery', JOURNAL OF PHYSIOLOGY-LONDON, 504 439-451 (1997)
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1996 |
Oba T, Koshita M, Van Helden DF, 'Modulation of frog skeletal muscle Ca2+ release channel gating by anion channel blockers.', The American journal of physiology, 271 C819-C824 (1996)
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Nova |
1996 |
Von der Weid PY, Van Helden DF, 'Beta-adrenoceptor-mediated hyperpolarization in lymphatic smooth muscle of guinea pig mesentery.', The American journal of physiology, 270 H1687-H1695 (1996)
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1996 |
Brent PJ, Pang G, Little G, Dosen PJ, VanHelden DF, 'The sigma receptor ligand, reduced haloperidol, induces apoptosis and increases intracellular-free calcium levels [Ca2+](i) in colon and mammary adenocarcinoma cells', BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 219 219-226 (1996)
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1996 |
Zipfel WR, OMalley JP, VanHelden D, Williams RM, Guild JB, Salpeter MM, Webb WW, 'Characterization of spontaneous calcium waves and sparks in primary cultures of fetal rat myotubes using two photon excitation point and line scanning microscopy.', BIOPHYSICAL JOURNAL, 70 WP283-WP283 (1996)
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Nova |
1996 |
Hashitani H, VanHelden DF, Suzuki H, 'Properties of spontaneous depolarizations in circular smooth muscle cells of rabbit urethra', BRITISH JOURNAL OF PHARMACOLOGY, 118 1627-1632 (1996)
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1996 |
vonderWeid PY, Crowe MJ, VanHelden DF, 'Endothelium-dependent modulation of pacemaking in lymphatic vessels of the guinea-pig mesentery', JOURNAL OF PHYSIOLOGY-LONDON, 493 563-575 (1996)
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1996 |
Stiles JR, VanHelden D, Bartol TM, Salpeter EE, Salpeter MM, 'Miniature endplate current rise times <100 mu s from improved dual recordings can be modeled with passive acetylcholine diffusion from a synaptic vesicle', PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 93 5747-5752 (1996)
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1996 |
Brock JA, VanHelden DF, Dosen P, Rush RA, 'Prevention of high blood pressure by reducing sympathetic innervation in the spontaneously hypertensive rat', JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM, 61 97-102 (1996)
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1996 |
vonderWeid PY, VanHelden DF, 'beta-Adrenoceptor-mediated hyperpolarization in lymphatic smooth muscle of guinea pig mesentery', AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 270 H1687-H1695 (1996)
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1996 |
Von Der Weid PY, Van Helden DF, 'ß-Adrenoceptor-mediated hyperpolarization in lymphatic smooth muscle of guinea pig mesentery', American Journal of Physiology - Heart and Circulatory Physiology, 270 (1996)
Intracellular microelectrode recordings were performed to investigate the consequences of ß-adrenoceptor activation in smooth muscle of guinea pig mesenteric lymphatic vessels. Is... [more]
Intracellular microelectrode recordings were performed to investigate the consequences of ß-adrenoceptor activation in smooth muscle of guinea pig mesenteric lymphatic vessels. Isoproterenol (Iso) hyperpolarized the membrane with an associated increase in membrane conductance and decreased the amplitude of spontaneous transient depolarizations. Iso effects were mimicked by forskolin (FSK), 3-isobutyl-1-methylxanthine, and two adenosine 3',5'- cyclic monophosphate (cAMP) derivatives. Iso- and FSK-induced hyperpolarizations were inhibited by H89, an inhibitor of cAMP-dependent protein kinase A, increased in K+-free solution, but were not affected by ouabain or by the nitric oxide synthase inhibitor N(¿)-nitro-L-arginine. They were partially inhibited by 20 mM tetraethylammonium (~40%) or by 2.5 mM 4-aminopyridine (~55%). The Iso-induced hyperpolarization was partially inhibited by iberiotoxin (20 nM) and charybdotoxin (40 nM), whereas the FSK- induced hyperpolarization was less affected. In cells where the Iso-induced hyperpolarization was decreased by 40 µM 1,2-bis(2-aminophenoxy)ethane- N,N,N',N'-tetraacetic acid, acetoxymethyl ester form, the FSK-induced hyperpolarization was little changed. Our results indicate that in guinea pig mesenteric lymphatic vessels, ß-adrenoceptor stimulation activates a protein kinase A-dependent K+ conductance, involving more than one channel type.
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Nova |
1996 |
Oba T, Koshita M, VanHelden DF, 'Modulation of frog skeletal muscle Ca2+ release channel gating by anion channel blockers', AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 271 C819-C824 (1996)
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1996 |
Oba T, Koshita M, Van Helden DF, 'Modulation of frog skeletal muscle Ca
Effects of niflumic acid and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) on frog skeletal muscle ryanodine receptors have been studied by incorporating sarco... [more]
Effects of niflumic acid and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) on frog skeletal muscle ryanodine receptors have been studied by incorporating sarcoplasmic reticulum vesicles into planar lipid bilayers. Niflumic acid increased the mean open probability (P(o)) at 10 µM and decreased P(o) at 100 µM with no change in open time constants, unitary conductance, and reversal potential. The P(o) was augmented by DIDS at 5-200 µM without affecting either unitary conductance or reversal potential. DIDS induced a new third open time constant, probably contributing to a long- lived open state. Channels modified by niflumic acid or DIDS still responded to Ca2+ release channel modulators. These results provide evidence that niflumic acid and DIDS modify the gating mechanism of ryanodine receptors without affecting binding sites to the modulators and the physical pathway of the conducting pore. p-Chloromercuriphenyl sulfonic acid (pCMPS) transiently increased the P(o). The channel modified by DIDS responded to pCMPS, whereas that by ryanodine did not. The long open state of the channel induced by DIDS is produced by a quite different mechanism(s) from that by ryanodine. Contrary to cardiac ryanodine receptors, P(o) of skeletal muscle channels was independent of voltage after DIDS modification.
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1995 |
BRENT PJ, DOSEN PJ, PANG G, VANHELDEN DF, 'THE SIGMA-BINDING SITE LIGAND, REDUCED HALOPERIDOL (RHAL), INCREASES INTRACELLULAR FREE CALCIUM LEVELS [CA2+]I IN COLON-CANCER CELLS', JOURNAL OF NEUROCHEMISTRY, 65 S13-S13 (1995) |
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Nova |
1995 |
BROCK JA, VANHELDEN DF, 'ENHANCED EXCITATORY JUNCTION POTENTIALS IN MESENTERIC-ARTERIES FROM SPONTANEOUSLY HYPERTENSIVE RATS', PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 430 901-908 (1995)
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1994 |
BATES RC, BURET A, VANHELDEN DF, HORTON MA, BURNS GF, 'APOPTOSIS INDUCED BY INHIBITION OF INTERCELLULAR CONTACT', JOURNAL OF CELL BIOLOGY, 125 403-415 (1994)
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1993 |
KLEMM MF, VANHELDEN DF, LUFF SE, 'ULTRASTRUCTURAL ANALYSIS OF SYMPATHETIC NEUROMUSCULAR-JUNCTIONS ON MESENTERIC VEINS OF THE GUINEA-PIG', JOURNAL OF COMPARATIVE NEUROLOGY, 334 159-167 (1993)
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Nova |
1993 |
VANHELDEN DF, 'PACEMAKER POTENTIALS IN LYMPHATIC SMOOTH-MUSCLE OF THE GUINEA-PIG MESENTERY', JOURNAL OF PHYSIOLOGY-LONDON, 471 465-479 (1993)
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1993 |
BERESFORDSMITH B, NESBITT KV, VANHELDEN DF, 'EDGE-DETECTION AT MULTIPLE LOCATIONS USING A RADAR TRACKING ALGORITHM AS EXEMPLIFIED IN ISOLATED GUINEA-PIG LYMPHATIC VESSELS', JOURNAL OF NEUROSCIENCE METHODS, 49 69-79 (1993)
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1991 |
VANHELDEN DF, 'SPONTANEOUS AND NORADRENALINE-INDUCED TRANSIENT DEPOLARIZATIONS IN THE SMOOTH-MUSCLE OF GUINEA-PIG MESENTERIC VEIN', JOURNAL OF PHYSIOLOGY-LONDON, 437 511-541 (1991)
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1990 |
VANHELDEN DF, WOOLRIDGE S, 'ROLE OF NERVES IN HYPERTENSION', NATURE, 348 118-119 (1990)
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1989 |
VANHELDEN DF, 'NORADRENALINE-INDUCED TRANSIENT DEPOLARIZATIONS IN THE SMOOTH-MUSCLE OF ISOLATED GUINEA-PIG MESENTERIC LYMPHATICS', JOURNAL OF PHYSIOLOGY-LONDON, 418 P173-P173 (1989)
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1988 |
VANHELDEN DF, 'ELECTROPHYSIOLOGY OF NEUROMUSCULAR-TRANSMISSION IN GUINEA-PIG MESENTERIC VEINS', JOURNAL OF PHYSIOLOGY-LONDON, 401 469-488 (1988)
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1988 |
VANHELDEN DF, 'AN ALPHA-ADRENOCEPTOR-MEDIATED CHLORIDE CONDUCTANCE IN MESENTERIC VEINS OF THE GUINEA-PIG', JOURNAL OF PHYSIOLOGY-LONDON, 401 489-501 (1988)
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1988 |
Van Helden DF, 'An alpha-adrenoceptor-mediated chloride conductance in mesenteric veins of the guinea-pig.', The Journal of Physiology, 401 489-501 (1988)
1. The ionic basis of the depolarizing responses resulting from ionophoresis of noradrenaline onto the smooth muscle of mesenteric veins has been investigated using electrically s... [more]
1. The ionic basis of the depolarizing responses resulting from ionophoresis of noradrenaline onto the smooth muscle of mesenteric veins has been investigated using electrically short segments of vessel. 2. Isolated cut segments of vein were effectively isopotential as assessed by the voltage response to a step change in current. The mean input resistance and time constant of the smooth muscle were 24 M omega and 131 ms respectively. 3. Data on the noradrenaline-induced slow depolarization indicated that it resulted from a decrease in conductance to potassium ions consistent with the finding of Suzuki (1981). 4. The fast noradrenaline-induced depolarization was found to have a reversal potential of about -22 mV. 5. Exposure to low-chloride solution caused greater than 90% suppression of this fast response with a 50% reduction occurring in less than 2 min. This suppression was not due to a negative shift in reversal potential. 6. The fast response underwent a large positive shift in reversal potential directly after changeover to low-chloride solution at times when any inactivation of the response was minimal. By contrast the fast response showed no evidence implicating either sodium or calcium as charge-carrying ions. 7. It is concluded the fast depolarization is carried by chloride ions. © 1988 The Physiological Society
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1986 |
HIRST GDS, SILVERBERG GD, VANHELDEN DF, 'THE ACTION-POTENTIAL AND UNDERLYING IONIC CURRENTS IN PROXIMAL RAT MIDDLE CEREBRAL ARTERIOLES', JOURNAL OF PHYSIOLOGY-LONDON, 371 289-304 (1986)
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Nova |
1986 |
HILL CE, HIRST GDS, SILVERBERG GD, VANHELDEN DF, 'SYMPATHETIC INNERVATION AND EXCITABILITY OF ARTERIOLES ORIGINATING FROM THE RAT MIDDLE CEREBRAL-ARTERY', JOURNAL OF PHYSIOLOGY-LONDON, 371 305-& (1986)
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1985 |
Hill CE, Hendry IA, Ngu MC, Van Helden DF, 'Subpopulations of sympathetic neurones differ in their sensitivity to nerve growth factor antiserum', Developmental Brain Research, 23 121-130 (1985)
Sympathetic postganglionic nerve fibres supplying mesenteric arteries and intrinsic ileal neurones differ in their characteristics of regeneration. Since the latter population of ... [more]
Sympathetic postganglionic nerve fibres supplying mesenteric arteries and intrinsic ileal neurones differ in their characteristics of regeneration. Since the latter population of neurones occurs predominantly in prevertebral ganglia, which have been reported to be spared to some extent after treatment with antiserum to nerve growth factor (anti-NGF), we have investigated whether the two populations were differentially sensitive to anti-NGF. Newborn rats were treated daily for the first postnatal week with either anti-NGF or 154 mM NaCl solution. At 4 and 8 weeks of age, the presence of a functional sympathetic innervation to the mesenteric arteries and the gut was determined and correlated with the fluorescence histochemical demonstration of noradrenergic fibres. At both ages, stimulation of extrinsic sympathetic fibres caused an inhibition of gut motility, while the mesenteric arteries completely lacked a sympathetic innervation. Retrograde labelling of nerve cell bodies in control and antiserum treated rats confirmed that the sympathetic neurones supplying the ileal neurones were located in the prevertebral, superior mesenteric and coeliac ganglia and in the splanchnic ganglia lying along the greater splanchnic nerves. By inference from retrograde labelling in control animals, sympathetic neurones supplying the mesenteric arteries were present in all these ganglia, as well as in the thoracic and lumbar paravertebral sympathetic chains. The results suggest that two functionally distinct populations of sympathetic neurones, which overlap considerably in their distributions, are differentially sensitive to the immunological postnatal removal of NGF. © 1985.
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1985 |
HIRST GDS, DEGLERIA S, VANHELDEN DF, 'NEUROMUSCULAR-TRANSMISSION IN ARTERIOLES', EXPERIENTIA, 41 874-879 (1985)
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Nova |
1985 |
TAYLOR WM, VANDEPOL E, VANHELDEN DF, REINHART PH, BYGRAVE FL, 'EFFECT OF DEPOLARIZING CONCENTRATIONS OF POTASSIUM ON CALCIUM-UPTAKE AND METABOLISM IN RAT-LIVER', FEBS LETTERS, 183 70-74 (1985)
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1985 |
HIRST GDS, JOHNSON SM, VANHELDEN DF, 'THE CALCIUM CURRENT IN A MYENTERIC NEURON OF THE GUINEA-PIG ILEUM', JOURNAL OF PHYSIOLOGY-LONDON, 361 297-314 (1985)
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1985 |
HIRST GDS, JOHNSON SM, VANHELDEN DF, 'THE SLOW CALCIUM-DEPENDENT POTASSIUM CURRENT IN A MYENTERIC NEURON OF THE GUINEA-PIG ILEUM', JOURNAL OF PHYSIOLOGY-LONDON, 361 315-337 (1985)
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Nova |
1985 |
HILL CE, HIRST GDS, NGU MC, VANHELDEN DF, 'SYMPATHETIC POSTGANGLIONIC REINNERVATION OF MESENTERIC-ARTERIES AND ENTERIC NEURONS OF THE ILEUM OF THE RAT', JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM, 14 317-334 (1985)
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1985 |
HILL CE, HENDRY IA, NGU MC, VANHELDEN DF, 'SUBPOPULATIONS OF SYMPATHETIC NEURONS DIFFER IN THEIR SENSITIVITY TO NERVE GROWTH-FACTOR ANTISERUM', DEVELOPMENTAL BRAIN RESEARCH, 23 121-130 (1985)
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1984 |
FINKEL AS, HIRST GDS, VANHELDEN DF, 'SOME PROPERTIES OF EXCITATORY JUNCTION CURRENTS RECORDED FROM SUBMUCOSAL ARTERIOLES OF GUINEA-PIG ILEUM', JOURNAL OF PHYSIOLOGY-LONDON, 351 87-98 (1984)
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1983 |
HILL CE, HIRST GDS, VANHELDEN DF, 'DEVELOPMENT OF SYMPATHETIC INNERVATION TO PROXIMAL AND DISTAL ARTERIES OF THE RAT MESENTERY', JOURNAL OF PHYSIOLOGY-LONDON, 338 129-147 (1983)
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1983 |
ARHEM P, VANHELDEN D, 'EFFECTS OF ALIPHATIC-ALCOHOLS ON MYELINATED NERVE MEMBRANE', ACTA PHYSIOLOGICA SCANDINAVICA, 119 105-107 (1983)
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Nova |
1982 |
HIRST GDS, VANHELDEN DF, 'IONIC BASIS OF THE RESTING POTENTIAL OF SUBMUCOSAL ARTERIOLES IN THE ILEUM OF THE GUINEA-PIG', JOURNAL OF PHYSIOLOGY-LONDON, 333 53-67 (1982)
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1982 |
GREEFF NG, KEYNES RD, VANHELDEN DF, 'FRACTIONATION OF THE ASYMMETRY CURRENT IN THE SQUID GIANT-AXON INTO INACTIVATING AND NON-INACTIVATING COMPONENTS', PROCEEDINGS OF THE ROYAL SOCIETY SERIES B-BIOLOGICAL SCIENCES, 215 375-389 (1982)
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1982 |
KEYNES RD, GREEFF NG, VANHELDEN DF, 'THE RELATIONSHIP BETWEEN THE INACTIVATING FRACTION OF THE ASYMMETRY CURRENT AND GATING OF THE SODIUM-CHANNEL IN THE SQUID GIANT-AXON', PROCEEDINGS OF THE ROYAL SOCIETY SERIES B-BIOLOGICAL SCIENCES, 215 391-404 (1982)
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1981 |
HARVEY AL, VANHELDEN DF, 'AGE-RELATED-CHANGES IN PROPERTIES OF ACETYLCHOLINE-RECEPTORS IN SINGLY AND MULTIPLY INNERVATED SKELETAL-MUSCLES OF THE CHICKEN', BRITISH JOURNAL OF PHARMACOLOGY, 74 P297-P298 (1981) |
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1981 |
HARVEY AL, VANHELDEN D, 'ACETYLCHOLINE-RECEPTORS IN SINGLY AND MULTIPLY INNERVATED SKELETAL-MUSCLE FIBERS OF THE CHICKEN DURING DEVELOPMENT', JOURNAL OF PHYSIOLOGY-LONDON, 317 397-411 (1981)
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1979 |
BARRY PH, GAGE PW, VANHELDEN DF, 'CATION PERMEATION AT THE AMPHIBIAN MOTOR ENDPLATE', JOURNAL OF MEMBRANE BIOLOGY, 45 245-276 (1979)
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1979 |
GAGE PW, HAMILL OP, VANHELDEN D, 'DUAL EFFECTS OF ETHER ON ENDPLATE CURRENTS', JOURNAL OF PHYSIOLOGY-LONDON, 287 353-369 (1979)
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1979 |
GAGE PW, VANHELDEN D, 'EFFECTS OF PERMEANT MONO-VALENT CATIONS ON ENDPLATE CHANNELS', JOURNAL OF PHYSIOLOGY-LONDON, 288 509-528 (1979)
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1979 |
KEYNES RD, MALACHOWSKI GC, VANHELDEN DF, 'EFFECT OF CALCIUM ON THE SODIUM GATING CURRENT IN THE SQUID GIANT-AXON', JOURNAL OF PHYSIOLOGY-LONDON, 295 P54-P55 (1979)
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1979 |
GAGE PW, HAMILL OP, VANHELDEN DF, BARRY PH, 'ACETYLCHOLINE RECEPTORS', MUSCLE & NERVE, 2 314-314 (1979) |
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1979 |
BARRY PH, GAGE PW, VANHELDEN DF, 'CATION PERMEATION THROUGH SINGLE MOTOR ENDPLATE CHANNELS', MUSCLE & NERVE, 2 314-314 (1979) |
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Nova |
1979 |
VANHELDEN DF, GAGE PW, HAMILL OP, 'CONDUCTANCE OF ENDPLATE CHANNELS IS VOLTAGE DEPENDENT', NEUROSCIENCE LETTERS, 11 227-232 (1979)
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1979 |
BARRY PH, GAGE PW, VANHELDEN DF, 'ENDPLATE CHANNELS BEHAVE AS NEUTRAL SITE CHANNELS', NEUROSCIENCE LETTERS, 11 233-237 (1979)
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1978 |
GAGE PW, MCBURNEY RN, VANHELDEN D, 'OCTANOL REDUCES ENDPLATE CHANNEL LIFETIME', JOURNAL OF PHYSIOLOGY-LONDON, 274 279-298 (1978)
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1977 |
VANHELDEN D, HAMILL OP, GAGE PW, 'PERMEANT CATIONS ALTER ENDPLATE CHANNEL CHARACTERISTICS', NATURE, 269 711-713 (1977)
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1974 |
GAGE PW, MCBURNEY RN, VANHELDE D, 'ENDPLATE CURRENTS ARE SHORTENED BY OCTANOL - POSSIBLE ROLE OF MEMBRANE LIPID', LIFE SCIENCES, 14 2277-2283 (1974)
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