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mM K+ (mm + k+)
Selected AbstractsDevelopmental changes in the modulation of respiratory rhythm generation by extracellular K+ in the isolated bullfrog brainstemDEVELOPMENTAL NEUROBIOLOGY, Issue 3 2003Rachel E. Winmill Abstract This study tested the hypothesis that voltage-dependent, respiratory-related activity in vitro, inferred from changes in [K+]o, changes during development in the amphibian brainstem. Respiratory-related neural activity was recorded from cranial nerve roots in isolated brainstem,spinal cord preparations from 7 premetamorphic tadpoles and 10 adults. Changes in fictive gill/lung activity in tadpoles and buccal/lung activity in adults were examined during superfusion with artificial CSF (aCSF) with [K+]o ranging from 1 to 12 mM (4 mM control). In tadpoles, both fictive gill burst frequency (fgill) and lung burst frequency (flung) were significantly dependent upon [K+]o (r2 > 0.75; p < 0.001) from 1 to 10 mM K+, and there was a strong correlation between fgill and flung (r2 = 0.65; p < 0.001). When [K+]o was raised to 12 mM, there was a reversible abolition of fictive breathing. In adults, fictive buccal frequency (fbuccal), was significantly dependent on [K+]o (r2 = 0.47; p < 0.001), but [K+]o had no effect on flung (p > 0.2), and there was no significant correlation between fbuccal and flung. These data suggest that the neural networks driving gill and lung burst activity in tadpoles may be strongly voltage modulated. In adults, buccal activity, the proposed remnant of gill ventilation in adults, also appears to be voltage dependent, but is not correlated with lung burst activity. These results suggest that lung burst activity in amphibians may shift from a "voltage-dependent" state to a "voltage-independent" state during development. This is consistent with the hypothesis that the fundamental mechanisms generating respiratory rhythm in the amphibian brainstem change during development. We hypothesize that lung respiratory rhythm generation in amphibians undergoes a developmental change from a pacemaker to network-driven process. © 2003 Wiley Periodicals, Inc. J Neurobiol 55: 278,287, 2003 [source] Structure,activity relationships of isoeugenol-based chlorophenylpiperazine derivatives on serotonergic/adrenergic receptor, platelet aggregation, and lipid peroxidationDRUG DEVELOPMENT RESEARCH, Issue 5 2010Kuo-Ping Shen Abstract Three isoeugenol-based eugenosedin chlorphenylpiperazine derivatives, Eu-A, Eu-B, and Eu-C, were synthesized and tested for their serotonergic, adrenergic antagonist, antioxidant, and anti-aggregation activities. In radioligand binding assays, all three agents displayed significant binding affinities on ,1, ,2, ,1, 5-HT1B, and 5-HT2A receptors. In human platelet, they inhibited epinephrine and 5-HT-induced aggregation, and in human platelet with ,2 and 5-HT2A receptors they had a competitive binding effect. Eu-B and Eu-C were more potent than Eu-A. All compounds had antioxidant effects derived from aryloxypropanolamine. Eu- A, Eu-B, or Eu-C (1, 3, 5,mg/kg iv) given to normotensive Wistar rats produced a dose-dependent decrease in mean arterial blood pressure and heart rate and when injected into the cisternum, Eu-A, Eu-B, or Eu-C (0.3, 0.03,µmol) increased blood pressure within 15,min. Pretreatment with any of the three agents inhibited clonidine (38,pmol)-induced hypotension. In vitro experiments, Eu-A, Eu-B, or Eu-C (1, 10, and 100,µM) competitively antagonized norepinephrine-, clonidine-, and 5-HT (10,8,10,4,M)-induced vasocontraction in isolated rat aorta, and competitively antagonized isoproterenol (10,8,10,4,M)-induced positive inotropic effects in a concentration-dependent manner in the isolated rat left atrium. In isolated rabbit ear arteries sensitized with 16,mM K+, all three agents antagonized 5-nonyloxytryptamine- and 5-HT-induced vasocontractions. These findings show that Eu-A, Eu-B, and Eu-C possess functional ,1, ,2, ,1, 5-HT1B, and 5-HT2A receptor blocking activities. In conclusion, the changes in the position of chloride at phenylpiperazine influenced the serotonergic receptor, adrenoceptor antagonistic activities, but not anti-aggregation and antioxidant activities. Drug Dev Res 71:1,9, 2010. © 2010 Wiley-Liss, Inc. [source] 2,2,-Nitrophenylisatogen potentiates P2X1 receptor mediated vascular contraction and blood pressure elevationDRUG DEVELOPMENT RESEARCH, Issue 1 2003Anna-Karin Wihlborg Abstract The objective of this research was to examine the effects of chemical compounds with possible P2 receptor modulating effects and to characterize the potentiating effects of 2,2,-nitrophenylisatogen (NPI) on P2X1 receptors in vitro and in vivo. Chemical compounds were tested in an in vitro pharmacological assay using vascular segments from the rat mesenteric artery stimulated by P2 receptor-specific agonists. Contractions were expressed as a percentage of 60 mM K+ -induced contractions. Blood pressure was evaluated in pithed rats. NPI (30 ,M) added 15 min before addition of the P2X1 receptor-specific agonist ,,-MeATP increased the maximum vasoconstriction from 23% to 49% (an increase of 113%). Furthermore, NPI prevented the desensitization of repeated ,,-MeATP contractions. Related compounds were examined, and 2-(3-methoxy-phenyl)-1-oxy-indol-3-one (MPI) had similar effects as NPI, but several others lacked effect. NPI had no effect on ADP,S (P2Y1) or acetylcholine-mediated vasodilatation, nor on UTP (P2Y2/4), UDP (P2Y6), or noradrenaline-mediated contractions. In pithed rats, the blood pressure response to 50 nmol/kg-infusion of ,,-MeATP was increased from 50±6 to 63±5 mmHg (P<0.05), but had no effect on basal blood pressure or on the cardiovascular response to preganglionic nerve stimulation. In conclusion, NPI and MPI potentiates P2X1 receptor vascular contractions in vitro and (NPI) blood pressure effects in vivo. It is possible that the effect is mediated by an inhibition of P2X1 receptor desensitization. Drug Dev. Res. 59:82,87, 2003. © 2003 Wiley-Liss, Inc. [source] Inhibitory effect of osmotic concentration, potassium and pH on motility of the sperm of the North American burbot Lota lota maculosaJOURNAL OF FISH BIOLOGY, Issue 1 2007M. D. Zuccarelli Seminal plasma factors maintaining North American (NA) burbot Lota lota maculosa sperm quiescent were examined. Sperm were diluted into buffered saline solutions of various compositions and motility assessed. After 1 h in these solutions at 10° C, aliquots of the suspension were diluted with tap water and motility again assessed. Dilution of sperm in an incubation solution containing Ca2+ in the absence of K+ initiated sperm motility resulting in low motility when sperm were subsequently diluted in tap water. Incubation solutions with osmolalities >200 mOsm kg,1 and containing 12·5 mM K+ prevented the onset of sperm motility and were associated with maximal sperm motility upon dilution in tap water. Sperm maintained at lower osmolalities exhibited limited motility upon dilution in tap water indicating interdependence between K+ and osmolality in maintaining sperm quiescent in the presence of Ca2+. Sperm kept in incubation solution at pH values < c. 7·5 for 1 h demonstrated reduced motility when subsequently diluted in tap water. That motility of sperm was pH sensitive was further indicated by CO2 inhibition of motility. Therefore, NA burbot sperm are probably maintained in an immotile state, yet with potential for motility, by combination of high K+, osmolality and possibly pH. The results from this study differ from published information on sperm quiescence in the temporally and geographically distinct Eurasian burbot Lota lota lota. [source] ,-Synuclein modulation of Ca2+ signaling in human neuroblastoma (SH-SY5Y) cellsJOURNAL OF NEUROCHEMISTRY, Issue 5 2009Nishani T. Hettiarachchi Abstract Parkinson's disease (PD) is characterized in part by the presence of ,-synuclein (,-syn) rich intracellular inclusions (Lewy bodies). Mutations and multiplication of the ,-synuclein gene (SNCA) are associated with familial PD. Since Ca2+ dyshomeostasis may play an important role in the pathogenesis of PD, we used fluorimetry in fura-2 loaded SH-SY5Y cells to monitor Ca2+ homeostasis in cells stably transfected with either wild-type ,-syn, the A53T mutant form, the S129D phosphomimetic mutant or with empty vector (which served as control). Voltage-gated Ca2+ influx evoked by exposure of cells to 50 mM K+ was enhanced in cells expressing all three forms of ,-syn, an effect which was due specifically to increased Ca2+ entry via L-type Ca2+ channels. Mobilization of Ca2+ by muscarine was not strikingly modified by any of the ,-syn forms, but they all reduced capacitative Ca2+ entry following store depletion caused either by muscarine or thapsigargin. Emptying of stores with cyclopiazonic acid caused similar rises of [Ca2+]i in all cells tested (with the exception of the S129D mutant), and mitochondrial Ca2+ content was unaffected by any form of ,-synuclein. However, only WT ,-syn transfected cells displayed significantly impaired viability. Our findings suggest that ,-syn regulates Ca2+ entry pathways and, consequently, that abnormal ,-syn levels may promote neuronal damage through dysregulation of Ca2+ homeostasis. [source] Activity-dependent somatostatin gene expression is regulated by cAMP-dependent protein kinase and Ca2+ -calmodulin kinase pathwaysJOURNAL OF NEUROSCIENCE RESEARCH, Issue 4 2010Isabel Sánchez-Muñoz Abstract Ca2+ influx through L-type voltage-gated Ca2+ channels (L-VSCC) is required for K+ -induced somatostatin (SS) mRNA. Increase in intracellular Ca2+ concentration leads to the activation of cyclic AMP-responsive element binding protein (CREB), a key regulator of SS gene transcription. Several different protein kinases possess the capability of driving CREB upon membrane depolarization. We investigated which of the signalling pathways involved in CREB activation mediates SS gene induction in response to membrane depolarization in cerebrocortical cells exposed to 56 mM K+. Activity dependent phosphorylation of CREB in Ser133 was immunodetected. Activation of CREB was biphasic showing two peaks at 5 and 60 min. The selective inhibitors of extracellular signal related protein kinase/mitogen-activated protein kinase (ERK/MAPK) PD098059, cyclic-AMPdependent protein kinase (cAMP/PKA) H89 and RpcAMPS, and Ca2+/calmodulin-dependent protein kinases (CaMKs) pathways KN62 and KN93 were used to determine the signalling pathways involved in CREB activation. Here we show that the early activation of CREB was dependent on cAMP/PKA along with CaMKs pathways whereas the ERK/MAPK and CaMKs were implicated in the second peak. We observed that H89, RpcAMPS, KN62 and KN93 blocked K+ -induced SS mRNA whereas PD098059 did not. These findings indicate that K+ -induced SSmRNA is mediated by the activation of cAMP/PKA and CaMKs pathways, thus suggesting that the early activation of CREB is involved in the induction of SS by neuronal activity. We also demonstrated, using transient transfections of cerebrocortical cells, that K+ induces the transcriptional regulation of the SS gene through the cAMP-responsive element (CRE) sequence located in the SS promoter. © 2009 Wiley-Liss, Inc. [source] Monetite (CaHPO4) Synthesis in Ethanol at Room TemperatureJOURNAL OF THE AMERICAN CERAMIC SOCIETY, Issue 12 2009A. Cuneyt Tas A straightforward process was developed to synthesize monetite (CaHPO4, dicalcium phosphate anhydrous) powders at room temperature (21°±1°C) in ethanol solutions. The process reported here constitutes an alternative to well-publicized monetite synthesis procedures based on the dehydration of brushite (CaHPO4·2H2O, dicalcium phosphate dihydrate) powders either in acidic, hot (70°,95°C) aqueous solutions or in drying ovens (200°,225°C). Submicrometer monetite powders were synthesized in ethanol (ethyl alcohol) solutions containing small aliquots of concentrated H3PO4 (orthophosphoric acid, 85%). Precipitated CaCO3 (calcium carbonate, calcite form) powders with submicrometer particles were simply stirred in the above solutions in glass bottles for 3 h. The starting Ca/P molar ratio in the synthesis bottles was 0.50. Monetite powders obtained with a stacked-nanosheets particle texture did not contain any unreacted CaCO3. Monetite powders were also found to have the ability to completely transform into apatitic (apatite-like) calcium phosphate powders when soaked in calcium-containing saline solutions (i.e., 142 mM Na+, 5 mM K+, and 50 mM Ca2+ in water) for 6 days at 37°C. [source] | ||||||||||