Cell membrane potential and resistance in liver.
Journal: 1979/March - Journal of Physiology
ISSN: 0022-3751
PUBMED: 731453
Abstract:
1. Isolated segments of mouse liver were placed in a Perspex bath through which physiological saline solutions of varying composition were circulated. Two microelectrodes were inserted in different liver cells under microscopic control allowing measurement of distance between the two micro-electrode tips. Current pulses were injected through one of these electrodes, causing electrotonic potential changes in nearby cells by current spread through intercellular junctions. These electrotonic potential changes were recorded with the second micro-electrode. The spatial decrement of the amplitude of the electrotonzpotential changes and their dependence on extracellular ion concentrations were analysed by three-dimensional cable analysis, modified to account for the geometry of the tissue. 2. During exposure to control solution the mean resting cell membrane potential was -37 mV, the space constant for intracellular current spread (lambda3 = square root of Rm/chrRi) was 390 micron and Ri, a measure which includes the intracellular resistivity and the junctional resistances, was 1.4 komegacm. From these values, and an estimate of tissue cell membrane density (chi) obtained by others, the specific membrane resistance (Rm) was calculated to be 5.1 komegacm2. 3. Replacement of extracellular Na+ by K+ resulted in a large depolarization and a large decrease in the membrane resistance. Replacement of extracellular Na+ by choline resulted in a small transient hyperpolarization and a small increase in the membrane resistance. Replacement of extracellular Cl- by methylsulphate or sulphate or of NaCl by sucrose resulted in a small transient depolarization and a large increase in the membrane resistance. 4. Glucagon (10(-7) M) and adrenaline (10(-5) M) evoked membrane hyperpolarization and reduction of membrane resistance (Rm). 5. The resting membrane ion conductance can be considered to consist of three components, Cl conductance (GCl), GK and GNa. The results suggest that GCl greater than GK greater than GNa. Changes in extracellular ion concentrations specifically alter the permeability properties of the cell membrane. The glucagon action can be explained in part by an increase in GK.
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J Physiol 284: 105-126

Cell membrane potential and resistance in liver.

Abstract

1. Isolated segments of mouse liver were placed in a Perspex bath through which physiological saline solutions of varying composition were circulated. Two microelectrodes were inserted in different liver cells under microscopic control allowing measurement of distance between the two micro-electrode tips. Current pulses were injected through one of these electrodes, causing electrotonic potential changes in nearby cells by current spread through intercellular junctions. These electrotonic potential changes were recorded with the second micro-electrode. The spatial decrement of the amplitude of the electrotonzpotential changes and their dependence on extracellular ion concentrations were analysed by three-dimensional cable analysis, modified to account for the geometry of the tissue. 2. During exposure to control solution the mean resting cell membrane potential was -37 mV, the space constant for intracellular current spread (lambda3 = square root of Rm/chrRi) was 390 micron and Ri, a measure which includes the intracellular resistivity and the junctional resistances, was 1.4 komegacm. From these values, and an estimate of tissue cell membrane density (chi) obtained by others, the specific membrane resistance (Rm) was calculated to be 5.1 komegacm2. 3. Replacement of extracellular Na+ by K+ resulted in a large depolarization and a large decrease in the membrane resistance. Replacement of extracellular Na+ by choline resulted in a small transient hyperpolarization and a small increase in the membrane resistance. Replacement of extracellular Cl- by methylsulphate or sulphate or of NaCl by sucrose resulted in a small transient depolarization and a large increase in the membrane resistance. 4. Glucagon (10(-7) M) and adrenaline (10(-5) M) evoked membrane hyperpolarization and reduction of membrane resistance (Rm). 5. The resting membrane ion conductance can be considered to consist of three components, Cl conductance (GCl), GK and GNa. The results suggest that GCl greater than GK greater than GNa. Changes in extracellular ion concentrations specifically alter the permeability properties of the cell membrane. The glucagon action can be explained in part by an increase in GK.

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  • Binder HJ, Boyer JL. Bile salts: a determinant of the bile-peritoneal electrical potential difference in the rat. Gastroenterology. 1973 Dec;65(6):943–948. [PubMed] [Google Scholar]
  • Blouin A, Bolender RP, Weibel ER. Distribution of organelles and membranes between hepatocytes and nonhepatocytes in the rat liver parenchyma. A stereological study. J Cell Biol. 1977 Feb;72(2):441–455.[PMC free article] [PubMed] [Google Scholar]
  • Brandt BL, Hagiwara S, Kidokoro Y, Miyazaki S. Action potentials in the rat chromaffin cell and effects of acetylcholine. J Physiol. 1976 Dec;263(3):417–439.[PMC free article] [PubMed] [Google Scholar]
  • Caillé JP, Schanne OF. Nombres de transport, t K , t Na et t Cl pour la membrane de la cellule hépatique in vivo. Can J Physiol Pharmacol. 1972 May;50(5):416–422. [PubMed] [Google Scholar]
  • Claret B, Claret M, Mazet JL. Ionic transport and membrane potential of rat liver cells in normal and low-chloride solutions. J Physiol. 1973 Apr;230(1):87–101.[PMC free article] [PubMed] [Google Scholar]
  • Claret M, Coraboeuf E, Favier MP. Effect of ionic concentration changes on membrane potential of perfused rat liver. Arch Int Physiol Biochim. 1970 Aug;78(3):531–545. [PubMed] [Google Scholar]
  • Claret M, Mazet JL. Ionic fluxes and permeabilities of cell membranes in rat liver. J Physiol. 1972 Jun;223(2):279–295.[PMC free article] [PubMed] [Google Scholar]
  • Claret M, Mazet JL. Transport passif de potassium dans les membranes plasmiques de cellules hépatiques. C R Acad Sci Hebd Seances Acad Sci D. 1972 Mar 27;274(13):1931–1934. [PubMed] [Google Scholar]
  • Claude P, Goodenough DA. Fracture faces of zonulae occludentes from "tight" and "leaky" epithelia. J Cell Biol. 1973 Aug;58(2):390–400.[PMC free article] [PubMed] [Google Scholar]
  • Friend DS, Gilula NB. Variations in tight and gap junctions in mammalian tissues. J Cell Biol. 1972 Jun;53(3):758–776.[PMC free article] [PubMed] [Google Scholar]
  • Graf J, Petersen OH. Electrogenic sodium pump in mouse liver parenchymal cells. Proc R Soc Lond B Biol Sci. 1974 Nov 5;187(1088):363–367. [PubMed] [Google Scholar]
  • Haylett DG, Jenkinson DH. Effects of noradrenaline on potassium reflux, membrane potential and electrolyte levels in tissue slices prepared from guinea-pig liver. J Physiol. 1972 Sep;225(3):721–750.[PMC free article] [PubMed] [Google Scholar]
  • Haylett DG, Jenkinson DH. The receptors concerned in the actions of catecholamines on glucose release, membrane potential and ion movements in guinea-pig liver. J Physiol. 1972 Sep;225(3):751–772.[PMC free article] [PubMed] [Google Scholar]
  • Heller P, Van der Kloot W. Transmembrane potentials in guinea-pig hepatocytes. J Physiol. 1974 Dec;243(3):577–598.[PMC free article] [PubMed] [Google Scholar]
  • HODGKIN AL. Ionic movements and electrical activity in giant nerve fibres. Proc R Soc Lond B Biol Sci. 1958 Jan 1;148(930):1–37. [PubMed] [Google Scholar]
  • HODGKIN AL, HOROWICZ P. The influence of potassium and chloride ions on the membrane potential of single muscle fibres. J Physiol. 1959 Oct;148:127–160.[PMC free article] [PubMed] [Google Scholar]
  • HODGKIN AL, KATZ B. The effect of sodium ions on the electrical activity of giant axon of the squid. J Physiol. 1949 Mar 1;108(1):37–77.[PMC free article] [PubMed] [Google Scholar]
  • Iwatsuki N, Petersen OH. In vitro action of bombesin on amylase secretion, membrane potential, and membrane resistance in rat and mouse pancreatic acinar cells. A comparison with other secretagogues. J Clin Invest. 1978 Jan;61(1):41–46.[PMC free article] [PubMed] [Google Scholar]
  • Iwatsuki N, Petersen OH. Membrane potential, resistance, and intercellular communication in the lacrimal gland: effects of acetylcholine and adrenaline. J Physiol. 1978 Feb;275:507–520.[PMC free article] [PubMed] [Google Scholar]
  • Kolb HA, Adam G. Regulation of ion permeabilities of isolated rat liver cells by external calcium concentration and temperature. J Membr Biol. 1976 Mar 18;26(2-3):121–151. [PubMed] [Google Scholar]
  • London CD, Diamond JM, Brooks FP. Electrical potential differences in the biliary tree. Biochim Biophys Acta. 1968 Apr 29;150(3):509–517. [PubMed] [Google Scholar]
  • Mazet JL, Claret M, Claret B. The passive transport of potassium in rat liver cells. J Membr Biol. 1974;18(3-4):335–350. [PubMed] [Google Scholar]
  • Nishiyama A, Petersen OH. Pancreatic acinar cells: membrane potential and resistance change evoked by acetylcholine. J Physiol. 1974 Apr;238(1):145–158.[PMC free article] [PubMed] [Google Scholar]
  • Petersen OH, Ueda N. Pancreatic acinar cells: effect of acetylcholine, pancreozymin, gastrin and secretin on membrane potential and resistance in vivo and in vitro. J Physiol. 1975 May;247(2):461–471.[PMC free article] [PubMed] [Google Scholar]
  • Purves RD. Current flow and potential in a three-dimensional syncytium. J Theor Biol. 1976 Jul 21;60(01):147–162. [PubMed] [Google Scholar]
  • Reuss L, Finn AL. Electrical properties of the cellular transepithelial pathway in Necturus gallbladder. I. Circuit analysis and steady-state effects of mucosal solution ionic substitutions. J Membr Biol. 1975 Dec 4;25(1-2):115–139. [PubMed] [Google Scholar]
  • Roberts ML, Petersen OH. Membrane potential and resistance changes induced in salivary gland acinar cells by microiontophoretic application of acetylcholine and adrenergic agonists. J Membr Biol. 1978 Mar 20;39(4):297–312. [PubMed] [Google Scholar]
  • Schanne O, Coraboeuf E. Potential and resistance measurements of rat liver cells in situ. Nature. 1966 Jun 25;210(5043):1390–1391. [PubMed] [Google Scholar]
  • Somlyo AP, Somlyo AV, Friedmann N. Cyclic adenosine monophosphate, cyclic guanosine monophosphate, and glucagon: effects on membrane potential and ion fluxes in the liver. Ann N Y Acad Sci. 1971 Dec 30;185:108–114. [PubMed] [Google Scholar]
  • Weibel ER, Stäubli W, Gnägi HR, Hess FA. Correlated morphometric and biochemical studies on the liver cell. I. Morphometric model, stereologic methods, and normal morphometric data for rat liver. J Cell Biol. 1969 Jul;42(1):68–91.[PMC free article] [PubMed] [Google Scholar]
  • Williams JA. Origin of transmembrane potentials in non-excitable cells. J Theor Biol. 1970 Aug;28(2):287–296. [PubMed] [Google Scholar]
Abstract
1. Isolated segments of mouse liver were placed in a Perspex bath through which physiological saline solutions of varying composition were circulated. Two microelectrodes were inserted in different liver cells under microscopic control allowing measurement of distance between the two micro-electrode tips. Current pulses were injected through one of these electrodes, causing electrotonic potential changes in nearby cells by current spread through intercellular junctions. These electrotonic potential changes were recorded with the second micro-electrode. The spatial decrement of the amplitude of the electrotonzpotential changes and their dependence on extracellular ion concentrations were analysed by three-dimensional cable analysis, modified to account for the geometry of the tissue. 2. During exposure to control solution the mean resting cell membrane potential was -37 mV, the space constant for intracellular current spread (lambda3 = square root of Rm/chrRi) was 390 micron and Ri, a measure which includes the intracellular resistivity and the junctional resistances, was 1.4 komegacm. From these values, and an estimate of tissue cell membrane density (chi) obtained by others, the specific membrane resistance (Rm) was calculated to be 5.1 komegacm2. 3. Replacement of extracellular Na+ by K+ resulted in a large depolarization and a large decrease in the membrane resistance. Replacement of extracellular Na+ by choline resulted in a small transient hyperpolarization and a small increase in the membrane resistance. Replacement of extracellular Cl- by methylsulphate or sulphate or of NaCl by sucrose resulted in a small transient depolarization and a large increase in the membrane resistance. 4. Glucagon (10(-7) M) and adrenaline (10(-5) M) evoked membrane hyperpolarization and reduction of membrane resistance (Rm). 5. The resting membrane ion conductance can be considered to consist of three components, Cl conductance (GCl), GK and GNa. The results suggest that GCl greater than GK greater than GNa. Changes in extracellular ion concentrations specifically alter the permeability properties of the cell membrane. The glucagon action can be explained in part by an increase in GK.
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