Ion-sensitive microelectrodes

2002 ◽  
Vol 2002 (2) ◽  
pp. 13
Keyword(s):  
Ion Sensitive Microelectrodes

Electrogenic, K + -dependent chloride transport in locust hindgut

1982 ◽  
Vol 299 (1097) ◽  
pp. 585-595 ◽  
Keyword(s):  
Chloride Transport ◽  
Passive Movement ◽  
Water Reabsorption ◽  
Experimental Conditions ◽  
Cl Transport ◽  
Neuropeptide Hormone ◽  
Flux Measurements ◽  
Ion Sensitive Microelectrodes ◽  
Voltage Clamping ◽  
Electrochemical Potentials

Potassium chloride is the major salt recycled in most insect excretory systems. Ion and water reabsorption occur in the rectum by active transport of Cl- and largely passive movement of K+. Both these processes are stimulated several fold by a neuropeptide hormone acting via cyclic AMP (cAMP). This Cl- transport process was investigated by using intracellular ion-sensitive microelectrodes, radiotracer flux measurements, voltage clamping, ion substitutions and inhibitors. The mucosal entry step for Cl- is energy-requiring and highly selective, and is stimulated directly by cAMP and luminal K +. Under some experimental conditions, measured electrochemical potentials for cations across the mucosal membrane are too small to drive Cl- entry by NaCl or KC1 cotransport mechanisms; moreover, net 36C1- flux is independent of the apical Na+ potential. Similarly no evidence for a HCO 3 -Cl- exchange was obtained. We conclude that Cl- transport in locust gut is different from mechanisms currently proposed for vertebrate tissues.

PII component of the toad electroretinogram

1992 ◽  
Vol 68 (1) ◽  
pp. 333-341 ◽  
Author(s):  
B. J. Katz ◽  
Z. Xu ◽  
J. Zheng ◽  
B. Oakley
Keyword(s):  
Excitatory Amino Acid ◽  
Cell Activity ◽  
Plexiform Layer ◽  
Müller Cell ◽  
Light Responses ◽  
M Wave ◽  
Cell Responses ◽  
Ion Sensitive Microelectrodes ◽  
Muller Cell ◽  
Dc Component

1. The PII component of the electroretinogram (ERG) is comprised of the b-wave and the DC component and is thought to reflect bipolar cell activity. Although the b-wave is generated in large part by a K+/Muller cell mechanism, the origin of the DC component is unclear. In this paper we detail our investigation of the origin of the DC component. We hypothesize that the DC component is generated by a K+/Muller cell mechanism identical to that involved in b-wave generation. 2. We studied the ERG in the dark-adapted, isolated retina preparation of the toad, Bu fo marinus. We used K+ ion-sensitive microelectrodes (K+ISM), as well as conventional intra- and extracellular microelectrodes, to record [K+]o changes, the vitreal ERG, and Muller cell responses. 3. We used the excitatory amino acid receptor agonist N-methyl-DL-aspartate (NMDLA) to inhibit light responses of third-order neurons and thereby eliminate most of the ERG M-wave. In the absence of the M-wave, the ERG consisted of PII and PIII. We then superfused the retina with a solution containing both kynurenic acid (KYN) and 2-amino-4-phosphonobutyric acid (APB), which together inhibit all retinal responses proximal to the photoreceptors. In the presence of KYN and APB, the ERG consisted only of PIII. Using digital subtraction, we reconstructed PII. To our knowledge, this is the first report of the isolation of a PII component in the ERG of a nonmammalian species. 4. Using K+ISMs, we recorded the distal K+ changes in the outer plexiform layer (OPL).(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanism and control of salt absorption in locust rectum

1983 ◽  
Vol 244 (2) ◽  
pp. R131-R142 ◽  
Author(s):  
J. Hanrahan ◽  
J. E. Phillips
Keyword(s):  
Apical Membrane ◽  
Electrical Coupling ◽  
Kinetic Studies ◽  
Malpighian Tubules ◽  
General Increase ◽  
Cl Transport ◽  
Ion Sensitive Microelectrodes ◽  
And Control ◽  
K Permeability ◽  
Camp Stimulation

The rectum is the main reabsorptive site in the excretory system of locusts. The primary urine entering this organ from the Malpighian tubules is rich in K+ (140 mM) and Cl- (90 mM), and most of this fluid is normally reabsorbed. Fluid and active Cl- reabsorption in the rectum are regulated by neuropeptide hormones from the corpus cardiacum. We have studied the mechanism of KCl reabsorption using voltage clamp, tracers, double-barreled ion-sensitive microelectrodes, and ion substitutions. Locust Cl- absorption differs from vertebrate systems in that it is not dependent on Na+ or HCO-3/CO2, and it is insensitive to normal inhibitors of Cl- transport. Entry of Cl- into rectal cells is active, electrogenic, and stimulated by luminal K+. This cation substantially increases the electrochemical gradient across the apical membrane against which Cl- is pumped; therefore K+ does not act solely and indirectly by electrical coupling. Kinetic studies also suggest that K+ activates the Cl- pump. Consequently at least two levels of control are exerted during cAMP stimulation; K+ permeability of the epithelium and the transepithelial potential generated by active Cl- transport both increase. The enhanced net K+ absorption from the lumen side after stimulation is largely passive, being electrically coupled to Cl- transport. However, this general increase in KCl absorption is "fine tuned" by K+ itself, through its direct effect on the Cl- pump.

Distribution and functional properties of glutamate receptors in the leech central nervous system

1996 ◽  
Vol 75 (6) ◽  
pp. 2312-2321 ◽  
Author(s):  
P. W. Dierkes ◽  
P. Hochstrate ◽  
W. R. Schlue
Keyword(s):  
Glutamate Receptors ◽  
Glial Cells ◽  
Membrane Depolarization ◽  
Free Solution ◽  
Fluorescent Indicators ◽  
Intracellular Na Activity ◽  
Bath Application ◽  
Voltage Dependent ◽  
Ion Sensitive Microelectrodes ◽  
Ca2 Channels

1. The effect of kainate and other glutamatergic agonists on the membrane potential (Em), the intracellular Na+ activity (aNai), and the intracellular free Ca2+ concentration ([Ca2+]i) of identified leech neurons and neuropile glial cells was measured with conventional and ion-sensitive microelectrodes, as well as with the use of the iontophoretically injected fluorescent indicators sodium-binding benzofuran isophthalate and Fura-2. 2. In Retzius neurons, AE, L, 8, and 101 motoneurons, and in the unclassified 50 neurons (Leydig cells) and AP neurons, as well as in neuropile glial cells, bath application of 100 microM kainate evoked a marked membrane depolarization and an increase in aNai and [Ca2+]i. The kainate-induced aNai increase persisted in solutions with high Mg2+ concentration in which synaptic transmission is blocked. 3. A membrane depolarization as well as an increase in aNai and [Ca2+]i was also evoked by L-glutamate, quisqualate, and L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA). The agonist-induced [Ca2+]i increase was inhibited by 6,7-dinitroquinoxaline-2,3-dione (DNQX). 4. In Ca(2+)-free solution, the kainate-induced [Ca2+]i increase was abolished in the neurons and in neuropile glial cells, whereas membrane depolarization and aNai increase were unchanged. In Na(+)-free solution, kainate had no effect on Em, aNai, or [Ca2+]i in the neurons. 5. In the mechanosensory T, P, and N neurons, kainate induced considerably smaller membrane depolarizations than in the other neurons or in neuropile glial cells, and it had no significant effect on aNai or [Ca2+]i. 6. It is concluded that in leech segmental ganglia the majority of the neurons and the neuropile glial cells, but probably not the mechanosensory neurons, possess glutamate receptors of the AMPA-kainate type. In the neurons, the [Ca2+]i increase caused by glutamatergic agonists is due to Ca2+ influx through voltage-dependent Ca2+ channels that are activated by the agonist-induced membrane depolarization.

An ion-sensitive microelectrode study on the effect of a high concentration of ivermectin on chloride balance in the somatic muscle bag cells of Ascaris suum

Parasitology ◽  
1993 ◽  
Vol 106 (4) ◽  
pp. 421-427 ◽  
Author(s):  
H. R. Parri ◽  
M. B. A. Djamgoz ◽  
L. Holden-Dye ◽  
R. J. Walker
Keyword(s):  
Receptor Antagonist ◽  
Chloride Channel ◽  
Gaba Receptor ◽  
Parasitic Nematode ◽  
Ascaris Suum ◽  
Muscle Cells ◽  
High Concentration ◽  
Somatic Muscle ◽  
Ion Sensitive Microelectrodes ◽  
Bag Cells

SUMMARYIvermectin has been shown to increase chloride conductances of invertebrate cells. On the muscle cells of the parasitic nematode Ascaris, ivermectin acts as both a GABA receptor antagonist and a chloride channel opener. In this study, ion-sensitive microelectrodes were used to investigate the effect of ivermectin on intracellular C1− concentration of the somatic muscle bag cells of Ascaris suum. Incubation of muscle cells with ivermectin (10 μM in 1% dimethyl sulphoxide vehicle for 60 min) increased intracellular C1− by 2·9 mM or 15% compared to controls (P > 0·01, n = 6).

scholarly journals Cellular mechanisms of potassium homeostasis in the mammalian nervous system

1987 ◽  
Vol 65 (5) ◽  
pp. 1038-1042 ◽  
Author(s):  
P. Grafe ◽  
K. Ballanyi
Keyword(s):  
Guinea Pig ◽  
Glial Cells ◽  
Sympathetic Ganglia ◽  
Olfactory Cortex ◽  
Lateral Olfactory Tract ◽  
Cellular Mechanisms ◽  
Potassium Homeostasis ◽  
Ion Sensitive Microelectrodes ◽  
Sympathetic Neurones ◽  
Intracellular Activities

Double-barrelled ion-sensitive microelectrodes were used to measure changes in the intracellular activities of K+, Na+, and Cl− (aKi, aNai, aCli) in neurones of rat sympathetic ganglia and in glial cells of slices from guinea-pig olfactory cortex. In sympathetic neurones, carbachol and γ-aminobutyric acid (GABA) produced a reversible decrease of aKi. The decrease of aKi during carbachol was accompanied by a rise of aNai, whereas in the presence of GABA decreases of aKi and aCli were seen. The reuptake of K+ released during the action of carbachol was completely blocked by ouabain, whereas furosemide inhibited the aKi recovery after the action of GABA. In glial cells, in contrast to the observations in the sympathetic neurones, aKi and aCli increased, whereas aNai decreased when neuronal activity was enhanced by repetitive stimulation of the lateral olfactory tract. It was found that barium ions and ouabain strongly reduced the activity-related rise of intraglial aKi in slices of guinea-pig olfactory cortex. These data show that mammalian neurones as well as glial cells possess several K+ uptake mechanisms that contribute to potassium homeostasis. Ouabain, furosemide, and Ba2+ are useful pharmacological tools to separate these mechanisms.

scholarly journals Methionine Sulfoximine, a Glutamine Synthetase Inhibitor, Attenuates Increased Extracellular Potassium Activity during Acute Hyperammonemia

1997 ◽  
Vol 17 (1) ◽  
pp. 44-49 ◽  
Author(s):  
Hideyoshi Sugimoto ◽  
Raymond C. Koehler ◽  
David A. Wilson ◽  
Saul W. Brusilow ◽  
Richard J. Traystman
Keyword(s):  
Glutamine Synthetase ◽  
Sodium Acetate ◽  
Ammonium Acetate ◽  
Ammonia Concentration ◽  
Methionine Sulfoximine ◽  
Extracellular Potassium ◽  
Edema Formation ◽  
Plasma Ammonia ◽  
Glutamine Synthesis ◽  
Ion Sensitive Microelectrodes

Hyperammonemia causes glutamine accumulation and astrocyte swelling. Inhibition of glutamine synthesis reduces ammonia-induced edema formation and watery swelling in astrocyte processes. Ordinarily, astrocytes tightly control extracellular K+ activity [K+]e. We tested the hypothesis that acute hyperammonemia interferes with this tight regulation such that [K+]e increases and that inhibition of glutamine synthetase reduces this increase in [K+]e. Ion-sensitive microelectrodes were used to measure [K+]e in parietal cortex continuously over a 6-h period in anesthetized rats. After i.v. sodium acetate infusion in eight control rats, plasma ammonia concentration was 33 ± 26 μmol/L (± SD) and [K+]e remained stable at 4.3 ± 1.6 mmol/L. During ammonium acetate infusion in nine rats, plasma ammonia increased to 594 ± 124 μmol/L at 2 h and to 628 ± 135 μmol/L at 6 h. There was a gradual increase in [K+]e from 3.9 ± 0.7 to 6.8 ± 2.7 mmol/L at 2 h and 11.8 ± 6.7 mmol/L at 6 h. In eight rats, L-methionine-D,L-sulfoximine (150 mg/kg) was infused 3 h before ammonium acetate infusion to inhibit glutamine synthetase. At 2 and 6 h of ammonium acetate infusion, plasma ammonia concentration was 727 ± 228 and 845 ± 326 μmol/L, and [K+]e was 4.5 ± 1.9 and 6.1 ± 3.8 mmol/L, respectively. The [K+]e value at 6 h was significantly less than that obtained with ammonium acetate infusion alone but was not different from that obtained with sodium acetate infusion. We conclude that acute hyperammonemia impairs astrocytic control of [K+]e and that this impairment is linked to glutamine accumulation rather than ammonium ions per se.

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