13 results on '"Hille B"'
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2. G protein-coupled mechanisms and nervous signaling
- Author
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Hille, B
- Published
- 1992
- Full Text
- View/download PDF
3. Modulation of high-voltage activated Ca(2+) channels by membrane phosphatidylinositol 4,5-bisphosphate.
- Author
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Suh BC, Leal K, and Hille B
- Subjects
- Adenosine Triphosphate analogs & derivatives, Adenosine Triphosphate metabolism, Adenosine Triphosphate pharmacology, Barium pharmacology, Biophysics, Calcium metabolism, Calcium Channels, L-Type genetics, Cell Line, Transformed, Chelating Agents pharmacology, Egtazic Acid analogs & derivatives, Egtazic Acid pharmacology, Electric Stimulation methods, Fluorescence Resonance Energy Transfer methods, Green Fluorescent Proteins genetics, Humans, Immunosuppressive Agents pharmacology, Ion Channel Gating drug effects, Ion Channel Gating genetics, Membrane Potentials drug effects, Membrane Potentials genetics, Muscarinic Agonists pharmacology, Oxotremorine pharmacology, Patch-Clamp Techniques methods, Phosphoric Monoester Hydrolases genetics, Phosphoric Monoester Hydrolases pharmacology, Sirolimus pharmacology, Time Factors, Transfection, Calcium Channels, L-Type physiology, Ion Channel Gating physiology, Phosphatidylinositol 4,5-Diphosphate metabolism
- Abstract
Modulation of voltage-gated Ca(2+) channels controls activities of excitable cells. We show that high-voltage activated Ca(2+) channels are regulated by membrane phosphatidylinositol 4,5-bisphosphate (PIP(2)) with different sensitivities. Plasma membrane PIP(2) depletion by rapamycin-induced translocation of an inositol lipid 5-phosphatase or by a voltage-sensitive 5-phosphatase (VSP) suppresses Ca(V)1.2 and Ca(V)1.3 channel currents by approximately 35% and Ca(V)2.1 and Ca(V)2.2 currents by 29% and 55%, respectively. Other Ca(V) channels are less sensitive. Inhibition is not relieved by strong depolarizing prepulses. It changes the voltage dependence of channel gating little. Recovery of currents from inhibition needs intracellular hydrolysable ATP, presumably for PIP(2) resynthesis. When PIP(2) is increased by overexpressing PIP 5-kinase, activation and inactivation of Ca(V)2.2 current slow and voltage-dependent gating shifts to slightly higher voltages. Thus, endogenous membrane PIP(2) supports high-voltage activated L-, N-, and P/Q-type Ca(2+) channels, and stimuli that activate phospholipase C deplete PIP(2) and reduce those Ca(2+) channel currents.
- Published
- 2010
- Full Text
- View/download PDF
4. Recovery from muscarinic modulation of M current channels requires phosphatidylinositol 4,5-bisphosphate synthesis.
- Author
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Suh BC and Hille B
- Subjects
- 1-Phosphatidylinositol 4-Kinase antagonists & inhibitors, 1-Phosphatidylinositol 4-Kinase metabolism, Adenosine Diphosphate metabolism, Adenosine Diphosphate pharmacology, Adenosine Triphosphate analogs & derivatives, Adenosine Triphosphate metabolism, Adenosine Triphosphate pharmacology, Animals, Cells, Cultured, Enzyme Inhibitors pharmacology, GTP-Binding Proteins drug effects, GTP-Binding Proteins metabolism, Glucose metabolism, Glucose pharmacology, KCNQ2 Potassium Channel, KCNQ3 Potassium Channel, Male, Membrane Potentials drug effects, Membrane Potentials physiology, Muscarinic Agonists pharmacology, Neural Inhibition drug effects, Neurons cytology, Neurons drug effects, Phosphorylation, Potassium Channels drug effects, Potassium Channels genetics, Potassium Channels, Voltage-Gated, Rats, Rats, Sprague-Dawley, Receptors, Muscarinic drug effects, Superior Cervical Ganglion cytology, Superior Cervical Ganglion drug effects, Synaptic Transmission drug effects, Synaptic Transmission physiology, Type C Phospholipases antagonists & inhibitors, Type C Phospholipases metabolism, Neural Inhibition physiology, Neurons metabolism, Phosphatidylinositol 4,5-Diphosphate biosynthesis, Potassium Channels metabolism, Receptors, Muscarinic metabolism, Superior Cervical Ganglion metabolism
- Abstract
Suppression of M current channels by muscarinic receptors enhances neuronal excitability. Little is known about the molecular mechanism of this inhibition except the requirement for a specific G protein and the involvement of an unidentified diffusible second messenger. We demonstrate here that intracellular ATP is required for recovery of KCNQ2/KCNQ3 current from muscarinic suppression, with an EC(50) of approximately 0.5 mM. Substitution of nonhydrolyzable ATP analogs for ATP slowed or prevented recovery. ADPbetaS but not ADP also prevented the recovery. Receptor-mediated inhibition was irreversible when recycling of agonist-sensitive pools of phosphatidylinositol-4,5-bisphosphate (PIP(2)) was blocked by lipid kinase inhibitors. Lipid phosphorylation by PI 4-kinase is required for recovery from muscarinic modulation of M current.
- Published
- 2002
- Full Text
- View/download PDF
5. Voltage-gated ion channels and electrical excitability.
- Author
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Armstrong CM and Hille B
- Subjects
- Animals, Electric Conductivity, Neurons chemistry, Ion Channel Gating physiology, Ion Channels physiology, Neurons physiology
- Published
- 1998
- Full Text
- View/download PDF
6. GABA(B)-mediated presynaptic inhibition of excitatory transmission and synaptic vesicle dynamics in cultured hippocampal neurons.
- Author
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Isaacson JS and Hille B
- Subjects
- 2-Amino-5-phosphonovalerate pharmacology, 6-Cyano-7-nitroquinoxaline-2,3-dione pharmacology, Action Potentials drug effects, Animals, Animals, Newborn, Cells, Cultured, Endocytosis, Evoked Potentials drug effects, Exocytosis, Fluorescent Dyes, Kinetics, Neurons drug effects, Patch-Clamp Techniques, Picrotoxin pharmacology, Pyridinium Compounds, Quaternary Ammonium Compounds, Rats, Spectrometry, Fluorescence, Synapses drug effects, Synaptic Vesicles drug effects, Baclofen pharmacology, Hippocampus physiology, Neurons physiology, Receptors, GABA-B physiology, Synapses physiology, Synaptic Vesicles physiology
- Abstract
Local recycling of synaptic vesicle membrane at nerve terminals is necessary to maintain a readily releasable pool of transmitter. To what extent are the dynamics of vesicle recycling subject to modulation? We examined the influence of presynaptic GABA(B) receptors on vesicle dynamics at single synapses using optical imaging of FM1-43 in cultured rat hippocampal neurons. The kinetics of FM1-43 destaining indicate that synapses from a single neuron have a unimodal distribution of release probabilities, and GABA(B)-mediated inhibition occurs uniformly at all sites. Electrical and optical recordings from single cells show that the inhibition of excitatory transmission is entirely accounted for by a rapidly reversible reduction of exocytosis. In contrast, GABA(B) receptors do not alter the rate or extent of endocytosis.
- Published
- 1997
- Full Text
- View/download PDF
7. Dominant role of mitochondria in clearance of large Ca2+ loads from rat adrenal chromaffin cells.
- Author
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Herrington J, Park YB, Babcock DF, and Hille B
- Subjects
- Adrenal Medulla cytology, Adrenal Medulla embryology, Animals, Biological Transport drug effects, Biological Transport, Active drug effects, Calcium Channel Blockers pharmacology, Calcium-Transporting ATPases antagonists & inhibitors, Carbonyl Cyanide m-Chlorophenyl Hydrazone pharmacology, Carrier Proteins antagonists & inhibitors, Cell Lineage, Cells, Cultured, Intracellular Fluid metabolism, Intracellular Membranes drug effects, Intracellular Membranes metabolism, Lanthanum pharmacology, Lithium pharmacology, Male, Membrane Potentials drug effects, Neural Crest, Neurons metabolism, Patch-Clamp Techniques, Rats, Rats, Sprague-Dawley, Sodium-Calcium Exchanger, Terpenes pharmacology, Tetraethylammonium, Tetraethylammonium Compounds pharmacology, Thapsigargin, Adrenal Medulla metabolism, Calcium metabolism, Calcium-Transporting ATPases metabolism, Carrier Proteins metabolism, Mitochondria physiology
- Abstract
Cytosolic Ca2+ (Ca2+c) clearance from adrenal chromaffin cells was studied by whole-cell patch clamp and indo-1 Ca2+ photometry after influx of Ca2+ through voltage-dependent Ca2+ channels. We isolated the rates of Ca2+c clearance by several mechanisms using combinations of the following agents (with their expected targets): Li+ or TEA substituted for Na+ (Na(+)-Ca2+ exchange), 1 mM La3+ applied after the depolarization (Na(+)-Ca2+ exchange and plasma membrane Ca(2+)-ATPase), 1 microM thapsigargin (pumping into reticular stores), and 2 microM carbonyl cyanide m-chlorophenylhydrazone (uptake into mitochondria). Remarkably, whenever [Ca2+]c rose above approximately 500 nM, Ca2+c clearance by mitochondria exceeded clearance by either Na(+)-Ca2+ exchange or the Ca2+ pumps of the plasma and reticular membranes. As [Ca2+]c fell again, Ca2+ reemerged from mitochondria, prolonging the final return to basal levels.
- Published
- 1996
- Full Text
- View/download PDF
8. Angiotensin II inhibits calcium and M current channels in rat sympathetic neurons via G proteins.
- Author
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Shapiro MS, Wollmuth LP, and Hille B
- Subjects
- Angiotensin Receptor Antagonists, Animals, Biphenyl Compounds pharmacology, Calcium Channels drug effects, Egtazic Acid analogs & derivatives, Egtazic Acid pharmacology, Ethylmaleimide pharmacology, Fluorescent Dyes, Guanosine Diphosphate analogs & derivatives, Guanosine Diphosphate pharmacology, Imidazoles pharmacology, In Vitro Techniques, Indoles, Ion Channels drug effects, Kinetics, Losartan, Membrane Potentials drug effects, Microscopy, Fluorescence, Neurons drug effects, Pertussis Toxin, Rats, Rats, Sprague-Dawley, Second Messenger Systems, Signal Transduction drug effects, Somatostatin pharmacology, Tetrazoles pharmacology, Thionucleotides pharmacology, Virulence Factors, Bordetella pharmacology, Angiotensin II pharmacology, Calcium metabolism, Calcium Channels physiology, GTP-Binding Proteins metabolism, Ion Channels physiology, Neurons physiology, Superior Cervical Ganglion physiology
- Abstract
We characterized inhibition of N-type Ca2+ and M current K+ channels in rat superior cervical ganglion neurons by angiotensin II (angioII) using the patch clamp. Of 120 neurons, 97 showed inhibition of ICa (mean 32%), which was slow in onset and very slow to reverse under whole-cell recording conditions. This inhibition was blocked by the AT1 receptor antagonist losartan, attenuated by inclusion of 2 mM GDP-beta-S in the pipette, mostly pertussis toxin insensitive, half-sensitive to N-ethylmaleimide, and wholly voltage independent. With 20 mM instead of 0.1 mM BAPTA in the pipette, the inhibition was strongly attenuated; however, we detected no angioII-induced [Ca2+]i signal using the fluorescent indicator indo-1. IBa from cell-attached patches was reduced by bath-applied angioII (mean 33%), suggesting use of a diffusible cytoplasmic messenger. M currents were inhibited by angioII in 8 of 11 neurons (mean 50%) cultured overnight. Hence, a second agonist, angioII, may share the slow, second messenger-utilizing, pertussis toxin-insensitive signaling pathway used by muscarinic agonists.
- Published
- 1994
- Full Text
- View/download PDF
9. Substance P and somatostatin inhibit calcium channels in rat sympathetic neurons via different G protein pathways.
- Author
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Shapiro MS and Hille B
- Subjects
- Animals, Calcium Channels physiology, Dialysis, Egtazic Acid analogs & derivatives, Egtazic Acid pharmacology, Electric Conductivity, Guanosine Diphosphate analogs & derivatives, Guanosine Diphosphate pharmacology, Male, Neurons drug effects, Pertussis Toxin, Rats, Rats, Sprague-Dawley, Receptors, Neurokinin-2, Receptors, Neurotransmitter physiology, Second Messenger Systems physiology, Thionucleotides pharmacology, Virulence Factors, Bordetella pharmacology, Calcium Channels drug effects, GTP-Binding Proteins physiology, Ganglia, Sympathetic cytology, Neurons physiology, Somatostatin pharmacology, Substance P pharmacology
- Abstract
We studied inhibition of N-type Ca2+ channels in rat superior cervical ganglion neurons by substance P (SP) and somatostatin-14 (Som). In whole-cell clamp, 70 of 82 acutely dissociated neurons showed inhibition (mean 37%) by 500 nM SP, and 54 of 61 showed inhibition by 240 nM Som (mean 57%). Pertussis toxin (PTX) blocked Som but not SP inhibition; intracellular dialysis with 2 mM GDP-beta-S attenuated inhibition with either peptide. Inhibition was voltage dependent with Som but not with SP. Neurokinin A (1 microM) or B was without effect, implicating NK1 tachykinin receptors. In cell-attached patches with bath-applied drugs, to test for a diffusible messenger, inhibition by SP or Som was only 8%. Thus, SP signaling is voltage independent and PTX insensitive; Som inhibition is voltage dependent and PTX sensitive; and both are membrane delimited.
- Published
- 1993
- Full Text
- View/download PDF
10. Inhibition of N- and L-type calcium channels by muscarinic receptor activation in rat sympathetic neurons.
- Author
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Mathie A, Bernheim L, and Hille B
- Subjects
- Animals, Calcium Channels drug effects, Dihydropyridines pharmacology, Electric Conductivity, Male, Norepinephrine pharmacology, Oxotremorine analogs & derivatives, Oxotremorine pharmacology, Rats, Rats, Inbred Strains, Receptors, Adrenergic, alpha drug effects, Receptors, Adrenergic, alpha physiology, Receptors, Muscarinic drug effects, Calcium Channels physiology, Ganglia, Sympathetic physiology, Neurons physiology, Receptors, Muscarinic physiology
- Abstract
Modulation of N- and L-type Ca2+ channels by oxotremorine-M (oxo-M) acting on muscarinic receptors and norepinephrine (NE) acting on alpha-adrenergic receptors was studied in superior cervical ganglion neurons. Oxo-M depresses dihydropyridine-augmented tail currents in whole-cell recordings, whereas NE does not. This modulation of L-type Ca2+ channels by oxo-M is abolished by adding 20 mM BAPTA to the pipette solution. Oxo-M, acting via a diffusible messenger, reduces the probability of opening of single N- and L-type channels recorded in cell-attached patches. We conclude that a diffusible messenger signaling pathway activated by oxo-M inhibits both N- and L-type Ca2+ channels, whereas a membrane-delimited pathway activated by oxo-M and NE inhibits only N-type Ca2+ channels.
- Published
- 1992
- Full Text
- View/download PDF
11. Pertussis toxin and voltage dependence distinguish multiple pathways modulating calcium channels of rat sympathetic neurons.
- Author
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Beech DJ, Bernheim L, and Hille B
- Subjects
- Adrenergic alpha-Agonists pharmacology, Animals, Electrophysiology, GTP-Binding Proteins physiology, Ion Channel Gating physiology, Male, Norepinephrine pharmacology, Oxotremorine pharmacology, Rats, Rats, Inbred Strains, Receptors, Muscarinic physiology, Calcium Channels physiology, Neurons physiology, Pertussis Toxin, Sympathetic Nervous System physiology, Virulence Factors, Bordetella pharmacology
- Abstract
Agonist-induced suppression of current in voltage-gated Ca2+ channels was studied in rat sympathetic neurons. We have previously distinguished two intracellular signaling pathways used by muscarinic agonists to suppress neuronal Ca2+ current-one fast and membrane delimited, the other slow and acting via a diffusible second messenger. We now show that the fast pathway is sensitive mainly to pertussis toxin and shifts the gating of Ca2+ channels to more positive voltages (voltage dependent). The slow pathway is pertussis toxin insensitive and depresses currents at all test potentials (voltage independent). Muscarinic agonists may also activate a pertussis toxin-insensitive fast pathway. alpha-Adrenergic agonists use the fast pertussis toxin-sensitive and the fast insensitive pathways, but not the slow one.
- Published
- 1992
- Full Text
- View/download PDF
12. A diffusible second messenger mediates one of the pathways coupling receptors to calcium channels in rat sympathetic neurons.
- Author
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Bernheim L, Beech DJ, and Hille B
- Subjects
- Animals, Egtazic Acid pharmacology, Electric Conductivity drug effects, In Vitro Techniques, Male, Membrane Potentials drug effects, Norepinephrine pharmacology, Oxotremorine pharmacology, Phorbol 12,13-Dibutyrate pharmacology, Rats, Rats, Inbred Strains, Receptors, Adrenergic, alpha drug effects, Receptors, Muscarinic drug effects, Calcium Channels physiology, Ganglia, Sympathetic physiology, Neurons physiology, Receptors, Adrenergic, alpha physiology, Receptors, Muscarinic physiology, Second Messenger Systems
- Abstract
Muscarinic and alpha-adrenergic suppression of current through Ca2+ channels was studied in adult rat superior cervical ganglion neurons using whole-cell and cell-attached configurations of the patch-clamp technique. Oxotremorine methiodide suppressed ICa by both a rapid (much less than 1 s) and a slow (greater than 4 s) process, whereas norepinephrine suppressed ICa only by a rapid process. The slow muscarinic suppression could be prevented by adding 20 mM BAPTA, a Ca2+ chelator, to the recording pipette, whereas the adrenergic suppression was not affected. Muscarinic, but not alpha-adrenergic, receptors can couple to Ca2+ channels by a second messenger capable of diffusing into an on-cell patch. This signal seems not to be carried by intracellular Ca2+, cGMP, cAMP, or protein kinase C.
- Published
- 1991
- Full Text
- View/download PDF
13. Agonists that suppress M-current elicit phosphoinositide turnover and Ca2+ transients, but these events do not explain M-current suppression.
- Author
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Pfaffinger PJ, Leibowitz MD, Subers EM, Nathanson NM, Almers W, and Hille B
- Subjects
- Animals, Atropine pharmacology, Benzofurans, Electric Conductivity, Enzyme Activation, Fluorescent Dyes, Fura-2, Ganglia, Sympathetic drug effects, In Vitro Techniques, Muscarine pharmacology, Neurons drug effects, Ranidae, Type C Phospholipases metabolism, Acetylcholine pharmacology, Calcium metabolism, Ganglia, Sympathetic physiology, Gonadotropin-Releasing Hormone pharmacology, Inositol Phosphates metabolism, Neurons physiology, Phosphatidylinositols metabolism, Substance P pharmacology
- Abstract
The hypothesis that acetylcholine, substance P, and LHRH suppress M-current by activating phospholipase C was tested. Each agonist caused turnover of phosphoinositide, as measured by release of inositol phosphates, and a modest transient rise in intracellular free Ca2+ ([ Ca2+]i), as determined with fura-2. Active phorbol esters depressed M-current only 50% and did not prevent further suppression by LHRH. M-current, its control by agonists, and its depression by phorbol esters were not affected by adding inositol trisphosphate or Ca2+ buffers with high or low Ca2+ to the whole-cell, voltage-clamp pipette. We conclude that phospholipase C activation does occur but does not mediate the suppression of M-current by agonists. Caffeine produced large [Ca2+]i transients and acted as an agonist to suppress M-current.
- Published
- 1988
- Full Text
- View/download PDF
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