scholarly journals Effect of external cation concentration and metabolic inhibitors on membrane potential of human glial cells.

1993 ◽  
Vol 460 (1) ◽  
pp. 365-383 ◽  
Author(s):  
T Brismar ◽  
V P Collins
Keyword(s):  
Membrane Potential ◽  
Glial Cells ◽  
Metabolic Inhibitors ◽  
Cation Concentration

External ions and membrane potential of leech neuropile glial cells

1982 ◽  
Vol 239 (1) ◽  
pp. 119-138 ◽  
Author(s):  
Wolfgang Walz ◽  
Wolf R. Schlue
Keyword(s):  
Membrane Potential ◽  
Glial Cells

Electrophysiological effects of GABA on cat pancreatic neurons

2001 ◽  
Vol 280 (3) ◽  
pp. G324-G331 ◽  
Author(s):  
L. Sha ◽  
S. M. Miller ◽  
J. H. Szurszewski
Keyword(s):  
Membrane Potential ◽  
Glial Cells ◽  
Channel Blocker ◽  
Islet Cells ◽  
Sympathetic Ganglia ◽  
Acid Decarboxylase ◽  
Protein Gene Product ◽  
Endogenous Gaba ◽  
Ganglion Neurons ◽  
Electrophysiological Effects

In mammalian peripheral sympathetic ganglia GABA acts presynaptically to facilitate cholinergic transmission and postsynaptically to depolarize membrane potential. The GABA effect on parasympathetic pancreatic ganglia is unknown. We aimed to determine the effect of locally applied GABA on cat pancreatic ganglion neurons. Ganglia with attached nerve trunks were isolated from cat pancreata. Conventional intracellular recording techniques were used to record electrical responses from ganglion neurons. GABA pressure microejection depolarized membrane potential with an amplitude of 17.4 ± 0.7 mV. Electrically evoked fast excitatory postsynaptic potentials were significantly inhibited (5.4 ± 0.3 to 2.9 ± 0.2 mV) after GABA application. GABA-evoked depolarizations were mimicked by the GABAA receptor agonist muscimol and abolished by the GABAA receptor antagonist bicuculline and the Cl− channel blocker picrotoxin. GABA was taken up and stored in ganglia during preincubation with 1 mM GABA; β-aminobutyric acid application after GABA loading significantly ( P < 0.05) increased depolarizing response to GABA (15.6 ± 1.0 vs. 7.8 ± 0.8 mV without GABA preincubation). Immunolabeling with antibodies to GABA, glial cell fibrillary acidic protein, protein gene product 9.5, and glutamic acid decarboxylase (GAD) immunoreactivity showed that GABA was present in glial cells, but not in neurons, and that glial cells did not contain GAD, whereas islet cells did. The data suggest that endogenous GABA released from ganglionic glial cells acts on pancreatic ganglion neurons through GABAA receptors.

scholarly journals Kinetic study of the plasma-membrane potential in procyclic and bloodstream forms of Trypanosoma brucei brucei using the fluorescent probe bisoxonol

1996 ◽  
Vol 314 (2) ◽  
pp. 595-601 ◽  
Author(s):  
Fabienne DEFRISE-QUERTAIN ◽  
Chantal FRASER-L'HOSTIS ◽  
Danièle CORAL ◽  
Jacques DESHUSSES
Keyword(s):  
Plasma Membrane ◽  
Membrane Potential ◽  
Trypanosoma Brucei ◽  
Cultured Cells ◽  
Bloodstream Form ◽  
Metabolic Inhibitors ◽  
Trypanosoma Brucei Brucei ◽  
Plasma Membrane Potential ◽  
Regulation Mechanisms ◽  
K Concentration

The characteristics of the plasma-membrane potential of procyclic and bloodstream forms of Trypanosoma brucei brucei (cultured cells) were investigated using the fluorescent anionic probe bisoxonol. Observation of a stable and representative plasma-membrane potential in the resting state required careful washing, centrifugation and maintenance of the cells at room temperature before measurement. Bloodstream forms were more prone to depolarization during washing at 4 °C than procyclic cells. The higher fluorescence observed in the presence of long slender cells than in the presence of procyclic cells shows that the plasma-membrane potential is more negative in the insect form. Healthy dilute cells can sustain their plasma-membrane potential for hours in the presence of external glucose. The presence of a high K+ concentration in the medium did not promote by itself the depolarization of either type of cell. Study of bisoxonol fluorescence as a function of time allowed us to follow the kinetics of the action of metabolic inhibitors in the presence of various ions. o-Vanadate (1 mM) was found to depolarize bloodstream-form cells rapidly but only in a phosphate-free NaCl buffer. Omeprazole and strophanthidin also specifically depolarized bloodstream-form trypanosomes. However, NN´-dicyclohexylcarbodi-imide depolarized both types of cell, but more rapidly for bloodstream-form cells. Bloodstream-form trypanosomes appear to use mainly a vanadate-sensitive Na+ pump to maintain their Na+-diffusion gradient. However, most of the ATPase inhibitors tested had little or no effect on the plasma-membrane potential of procyclics suggesting that this form of trypanosome may rely on several regulation mechanisms.

scholarly journals Studies on the efflux of metalloporphyrin from isolated rat liver mitochondria. Effect of respiratory substrates and metabolic inhibitors

1982 ◽  
Vol 202 (1) ◽  
pp. 41-46 ◽  
Author(s):  
P Husby ◽  
I Romslo
Keyword(s):  
Membrane Potential ◽  
Rat Liver ◽  
Incubation Medium ◽  
Energy State ◽  
Liver Mitochondria ◽  
Metabolic Inhibitors ◽  
Rat Liver Mitochondria ◽  
Isolated Rat Liver ◽  
Isolated Rat

Intramitochondrially synthesized Co-deuteroporphyrin is released to the incubation medium at a rate inversely correlated to the energy state of the mitochondria; i.e. the rate of efflux increases when substrate is depleted, respiration inhibited or the mitochondria are uncoupled. The efflux of Co-deuteroporphyrin from mitochondria remains low as long as the residual membrane potential is above one-third that of maximally energized mitochondria. Globin enhances the efflux of Co-deuteroporphyrin not only from mitochondria depleted of substrates [Husby & Romslo (1980) Biochem. J. 188, 459-465], but also from maximally energized mitochondria. The results provide further evidence for a co-operative mechanism between the mitochondria and their surroundings for the mobilization of metalloporphyrin from mitochondria.

scholarly journals Membrane potential of Plasmodium-infected erythrocytes.

1982 ◽  
Vol 93 (3) ◽  
pp. 685-689 ◽  
Author(s):  
R B Mikkelsen ◽  
K Tanabe ◽  
D F Wallach
Keyword(s):  
Membrane Potential ◽  
Plasma Membranes ◽  
Metabolic Inhibitors ◽  
Erythrocyte Membranes ◽  
Weak Acids ◽  
Atpase Inhibitor ◽  
Lipophilic Anion ◽  
Parasite Stage ◽  
Infected Cells ◽  
Electrogenic Proton Pump

The membrane potential (Em) of normal and Plasmodium chabaudi-infected rat erythrocytes was determined from the transmembrane distributions of the lipophilic anion, thiocyanate (SCN), and cation, triphenylmethylphosphonium (TPMP). The SCN- and TPMP-measured Em of normal erythrocytes are -6.5 +/- 3 mV and -10 +/- 4 mV, respectively. The TPMP-measured Em of infected cells depended on parasite developmental stage; "late" stages (schizonts and gametocytes) were characterized by a Em = -35 mV "early stages (ring and copurifying noninfected) by a low Em (-16 mV). The SCN-determined Em of infected cells was -7 mV regardless of parasite stage. Studies with different metabolic inhibitors including antimycin A, a proton ionophore (carbonylcyanide m-chlorophenylhydrazone [CCCP] ), and a H+ -ATPase inhibitor (N,N'-dicyclohexylcarbodiimide, [DCCD] ) indicate that SCN monitors the Em across the erythrocyte membrane of infected and normal cells whereas TPMP accumulation reflects the Em across the plasma membranes of both erythrocyte and parasite. These inhibitor studies also implicated proton fluxes in Em-generation of parasitized cells. Experiments with weak acids and bases to measure intracellular pH further support this proposal. Methylamine distribution and direct pH measurement after saponin lysis of erythrocyte membranes demonstrated an acidic pH for the erythrocyte matrix of infected cells. The transmembrane distributions of weak acids (acetate and 5,5-dimethyloxazolidine-2,4-dione) indicated a DCCD-sensitive alkaline compartment. The combined results suggest that the intraerythrocyte parasite Em and delta pH are in part the consequence of an electrogenic proton pump localized to the parasite plasma membrane.

Intracellular Ca2+ release mediated by metabotropic glutamate receptor activation in the leech giant glial cell.

1997 ◽  
Vol 200 (19) ◽  
pp. 2565-2573
Author(s):  
C Lohr ◽  
J W Deitmer
Keyword(s):  
Membrane Potential ◽  
Glutamate Receptors ◽  
Glutamate Receptor ◽  
Glial Cells ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate Receptor ◽  
Cyclopiazonic Acid ◽  
Receptor Activation ◽  
Atpase Inhibitor ◽  
Metabotropic Glutamate

We have investigated the effects of glutamate and glutamate receptor ligands on the intracellular free Ca2+ concentration ([Ca2+]i) and the membrane potential (Em) of single, identified neuropile glial cells in the central nervous system of the leech Hirudo medicinalis. Exposed glial cells of isolated ganglia were filled iontophoretically with the Ca2+ indicator dye Fura-2. Application of glutamate (200-500 mumoll-1) caused biphasic membrane potential shifts and increases in [Ca2+]i, which were only partly reduced by either removing extracellular Ca2+ or blocking ionotropic glutamate receptors with 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 50-100 mumol l-1. Metabotropic glutamate receptor (mGluR) ligands had the following rank of potency in inducing a rise in [Ca2+]i: quisqualate (QQ, 200 mumol l-1) &gt; glutamate (200 mumol l-1) &gt; L(+)2-amino-3-phosphonopropionic acid (L-AP3, 200 mumol l-1 &gt; trans-1-aminocyclopentane-1,3-dicarboxylic acid (t-ACPD, 400 mumol l-1). The mGluR-selective antagonist (RS)-alpha-methyl-4-carboxyphenylglycine [(RS)-MCPG, 1 mmol l-1] significantly reduced glutamate-evoked increases in [Ca2+]i by 20%. Incubation of the ganglia with the endoplasmic ATPase inhibitor cyclopiazonic acid (CPA, 10 mumol l-1) caused a significant (53%) reduction of glutamate-induced [Ca2+]i transients, while incubation with lithium ions (2 mmol l-1) resulted in a 46% reduction. The effects of depleting the Ca2+ stores with CPA and of CNQX were additive. We conclude that glutamate-induced [Ca2+]i transients were mediated by activation of both Ca(2+)-permeable ionotropic non-NMDA receptors and of metabotropic glutamate receptors leading to Ca2+ release from intracellular Ca2+ stores.

Potassium efflux of squid giant axons in low external divalent cation

1963 ◽  
Vol 204 (3) ◽  
pp. 480-482 ◽  
Author(s):  
Raymond J. Lipicky ◽  
S. H. Bryant
Keyword(s):  
Membrane Potential ◽  
Divalent Cation ◽  
Membrane Potentials ◽  
Resting Membrane Potential ◽  
Potassium Efflux ◽  
Giant Axons ◽  
Cation Concentration

In squid ( Loligo pealii) giant axons, potassium efflux was measured after soak-loading during washout, and membrane potentials were monitored using an intracellular pipette electrode. As external divalent cation is lowered down to 1/10 of normal, there is little change of resting potassium efflux or resting membrane potential (slight hyperpolarization), despite a tendency of the axon to fire repetitively. Below this concentration, efflux rises as much as eight times the normal 265 pmole·cm–2·sec–1 and potential falls (from 55 as far as 32 mv), inexcitability occurring at about 1/100 of normal external divalent cation concentration.

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