The Experts below are selected from a list of 282 Experts worldwide ranked by ideXlab platform
Sue C Kinnamon - One of the best experts on this subject based on the ideXlab platform.
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sweet taste transduction in hamster sweeteners and Cyclic Nucleotides depolarize taste cells by reducing a k current
Journal of Neurophysiology, 1996Co-Authors: T A Cummings, C Daniels, Sue C KinnamonAbstract:1. The gigaseal voltage-clamp technique was used to record responses of hamster taste receptor cells to synthetic sweeteners and Cyclic Nucleotides. Voltage-dependent currents and steady-state curr...
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sweet taste transduction in hamster taste cells evidence for the role of Cyclic Nucleotides
Journal of Neurophysiology, 1993Co-Authors: T A Cummings, J Powell, Sue C KinnamonAbstract:1. Physiological and behavioral responses to artificial sweeteners, natural sweeteners, and Cyclic Nucleotides were assessed using two techniques. An extracellular "in situ" technique recorded action potentials from fungiform taste buds and the two-bottle preference test measured behavioral preferences for the different sweeteners. 2. Two high-potency sweeteners, NC-00274-01 (NC01) and NC-00044-AA (NCAA), were preferred over water at micromolar concentrations. Saccharin and sucrose were likewise preferred, but at millimolar concentrations. 3. Bursts of action currents were elicited by sucrose at 200 mM, saccharin at 20 mM, and NCAA at 0.1 mM. A concentration-response curve for the high-potency sweetener NC01 revealed a threshold concentration of 1 microM and a saturation concentration of 100 microM. No responses were elicited by aspartame. 4. The responses to different sweeteners adapted rapidly at saturating concentrations. With NC01, adaptation was concentration dependent: at threshold the response adapted very slowly if at all. Adaptation increased with increasing concentration. 5. Membrane-permeant analogues of adenosine 3',5'-Cyclic monophosphate and guanosine 3',5'-Cyclic monophosphate mimicked sweeteners in their ability to elicit a response. This occurred with high fidelity: nearly every taste bud that responded to sweeteners also responded to the Nucleotides and every sweet-unresponsive taste bud was nucleotide unresponsive. 6. The sweet responses and nucleotide responses occurred in the absence of permeant apical cations and were not enhanced nor diminished by the presence of such cations. Amiloride had no effect on the sweet response.
T A Cummings - One of the best experts on this subject based on the ideXlab platform.
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sweet taste transduction in hamster sweeteners and Cyclic Nucleotides depolarize taste cells by reducing a k current
Journal of Neurophysiology, 1996Co-Authors: T A Cummings, C Daniels, Sue C KinnamonAbstract:1. The gigaseal voltage-clamp technique was used to record responses of hamster taste receptor cells to synthetic sweeteners and Cyclic Nucleotides. Voltage-dependent currents and steady-state curr...
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sweet taste transduction in hamster taste cells evidence for the role of Cyclic Nucleotides
Journal of Neurophysiology, 1993Co-Authors: T A Cummings, J Powell, Sue C KinnamonAbstract:1. Physiological and behavioral responses to artificial sweeteners, natural sweeteners, and Cyclic Nucleotides were assessed using two techniques. An extracellular "in situ" technique recorded action potentials from fungiform taste buds and the two-bottle preference test measured behavioral preferences for the different sweeteners. 2. Two high-potency sweeteners, NC-00274-01 (NC01) and NC-00044-AA (NCAA), were preferred over water at micromolar concentrations. Saccharin and sucrose were likewise preferred, but at millimolar concentrations. 3. Bursts of action currents were elicited by sucrose at 200 mM, saccharin at 20 mM, and NCAA at 0.1 mM. A concentration-response curve for the high-potency sweetener NC01 revealed a threshold concentration of 1 microM and a saturation concentration of 100 microM. No responses were elicited by aspartame. 4. The responses to different sweeteners adapted rapidly at saturating concentrations. With NC01, adaptation was concentration dependent: at threshold the response adapted very slowly if at all. Adaptation increased with increasing concentration. 5. Membrane-permeant analogues of adenosine 3',5'-Cyclic monophosphate and guanosine 3',5'-Cyclic monophosphate mimicked sweeteners in their ability to elicit a response. This occurred with high fidelity: nearly every taste bud that responded to sweeteners also responded to the Nucleotides and every sweet-unresponsive taste bud was nucleotide unresponsive. 6. The sweet responses and nucleotide responses occurred in the absence of permeant apical cations and were not enhanced nor diminished by the presence of such cations. Amiloride had no effect on the sweet response.
Timothy R Billiar - One of the best experts on this subject based on the ideXlab platform.
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Cyclic Nucleotides suppress tumor necrosis factor α mediated apoptosis by inhibiting caspase activation and cytochrome crelease in primary hepatocytes via a mechanism independent of akt activation
Journal of Biological Chemistry, 2000Co-Authors: Sufang Yang, Timothy R BilliarAbstract:Cyclic Nucleotides have been previously shown to modulate cell death processes in many cell types; however, the mechanisms by which Cyclic Nucleotides regulate apoptosis are unclear. In this study, we demonstrated that cAMP as well as cGMP analogs suppressed tumor necrosis factor α (TNFα) plus actinomycin D (ActD)-induced apoptosis in a dose-dependent manner in cultured primary hepatocytes. Furthermore, forskolin, which increases intracellular cAMP levels, also effectively suppressed TNFα+ActD-induced apoptosis. Activation of multiple caspases was suppressed in cells exposed to TNFα+ActD in the presence of cAMP or cGMP analogs. TNFα+ActD-induced cytochrome c release from mitochondria was also inhibited by cAMP or cGMP, reinforcing our conclusion that Cyclic Nucleotides interfere with the early signaling events of TNFα-mediated apoptosis. We evaluated the possibility that cAMP and cGMP inhibit apoptosis by activating the serine/threonine kinase Akt, which is known to promote cell survival. Both cAMP- and cGMP-elevating agents led to marked increases in Akt activation that was inhibited by the phosphatidylinositol 3′-kinase inhibitors, LY294002 and wortmannin. However, complete inhibition of Cyclic nucleotide-induced Akt activation had little effect on Cyclic nucleotide-mediated cell survival, indicating the existence of other survival pathways. Interestingly, the specific inhibitor of protein kinase A (PKA), KT5720, blocked cGMP-mediated protection but only partially prevented the anti-apoptotic effect of cAMP, indicating that both PKA-dependent and -independent mechanisms are involved in cAMP-mediated suppression of apoptosis signaling. Our data suggest that multiple survival signaling pathways coexist in cells and that Cyclic Nucleotides delay apoptosis by interfering with apoptosis signaling by both PKA-dependent and -independent mechanisms.
Hanschristian Pape - One of the best experts on this subject based on the ideXlab platform.
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modulation of hyperpolarization activated inward current and thalamic activity modes by different Cyclic Nucleotides
Frontiers in Cellular Neuroscience, 2018Co-Authors: Maia Datunashvili, Rahul Chaudhary, Mehrnoush Zobeiri, Annika Luttjohann, Evanthia Mergia, Arnd Baumann, Sabine Balfanz, Bjorn Budde, Gilles Van Luijtelaar, Hanschristian PapeAbstract:The hyperpolarization-activated inward current, Ih, plays a key role in the generation of rhythmic activities in thalamocortical relay (TC) neurons. Cyclic Nucleotides, like 3’, 5’-Cyclic adenosine monophosphate (cAMP), facilitate voltage-dependent activation of HCN channels by shifting the activation curve of Ih to more positive values and thereby terminating the rhythmic burst activity. The role of 3’, 5’- Cyclic guanosine monophosphate (cGMP) in modulation of Ih is not well understood. To determine the possible role of the NO-sensitive cGMP-forming guanylyl cyclase 2 (NO-GC2) to the control of thalamic Ih, the voltage-dependency and cGMP/cAMP-sensitivity of Ih was analyzed in TC neurons of the dorsal part of the lateral geniculate nucleus (dLGN) in WT and NO-GC2-deficit (NO-GC2-/-) mice. Whole cell voltage clamp recordings in brain slices revealed a more hyperpolarized half maximal activation (V1/2) of Ih in NO-GC2-/- TC neurons compared to wild type (WT). Different concentrations of 8-Br-cAMP / 8-Br-cGMP induced dose-dependent positive shifts of V1/2 in both strains. Treatment of WT slices with lyase enzyme inhibitors (SQ22536 and ODQ) resulted in further hyperpolarized V1/2. Under current clamp conditions NO-GC2-/- neurons exhibited a reduction in the Ih-dependent voltage sag and reduced action potential firing with hyperpolarizing and depolarizing current steps, respectively. Intrathalamic rhythmic bursting activity in brain slices and in a simplified mathematical model of the thalamic network was reduced in the absence of NO-GC2. In freely behaving NO-GC2-/- mice, delta and theta band activity was enhanced during active wakefulness (AW) and rapid eye movement sleep (REM) in cortical local field potential (LFP) in comparison to WT. These findings indicate that cGMP facilitates Ih activation and contributes to a tonic activity in TC neurons. On the network level basal cGMP production supports fast rhythmic activity in the cortex.
J Powell - One of the best experts on this subject based on the ideXlab platform.
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sweet taste transduction in hamster taste cells evidence for the role of Cyclic Nucleotides
Journal of Neurophysiology, 1993Co-Authors: T A Cummings, J Powell, Sue C KinnamonAbstract:1. Physiological and behavioral responses to artificial sweeteners, natural sweeteners, and Cyclic Nucleotides were assessed using two techniques. An extracellular "in situ" technique recorded action potentials from fungiform taste buds and the two-bottle preference test measured behavioral preferences for the different sweeteners. 2. Two high-potency sweeteners, NC-00274-01 (NC01) and NC-00044-AA (NCAA), were preferred over water at micromolar concentrations. Saccharin and sucrose were likewise preferred, but at millimolar concentrations. 3. Bursts of action currents were elicited by sucrose at 200 mM, saccharin at 20 mM, and NCAA at 0.1 mM. A concentration-response curve for the high-potency sweetener NC01 revealed a threshold concentration of 1 microM and a saturation concentration of 100 microM. No responses were elicited by aspartame. 4. The responses to different sweeteners adapted rapidly at saturating concentrations. With NC01, adaptation was concentration dependent: at threshold the response adapted very slowly if at all. Adaptation increased with increasing concentration. 5. Membrane-permeant analogues of adenosine 3',5'-Cyclic monophosphate and guanosine 3',5'-Cyclic monophosphate mimicked sweeteners in their ability to elicit a response. This occurred with high fidelity: nearly every taste bud that responded to sweeteners also responded to the Nucleotides and every sweet-unresponsive taste bud was nucleotide unresponsive. 6. The sweet responses and nucleotide responses occurred in the absence of permeant apical cations and were not enhanced nor diminished by the presence of such cations. Amiloride had no effect on the sweet response.
