Glial membrane potentials and their relationship to [K+]o in man and guinea pig

1981 ◽  
Vol 55 (3) ◽  
pp. 347-363 ◽  
Author(s):  
Selwyn Picker ◽  
Carl F. Pieper ◽  
Sidney Goldring
Keyword(s):  
Glioblastoma Multiforme ◽  
Guinea Pig ◽  
Focal Epilepsy ◽  
Brain Slices ◽  
Physiological Data ◽  
Resting Membrane Potential ◽  
Extracellular Potassium ◽  
Reactive Glia ◽  
Normal Human ◽  
The Mean

✓ Glial cells were studied in vitro in physiologically viable brain slices prepared from tissues obtained during operations for focal epilepsy and brain tumors. The results from human normal and reactive cerebral cortex and glial tumors were compared with those obtained in guinea pig cortex. The resting membrane potential (RMP) or the relationship of RMP to changes in extracellular potassium concentration ([K+]o) were recorded, and the cell was injected iontophoretically with horseradish peroxidase (HRP) for later visualization and correlation with the physiological data. In normal cortex, the marked cells were protoplasmic astrocytes; in reactive cortex, fibrous astrocytes with abnormal processes predominated. The majority of neoplastic glia resembled the reactive astrocytes, except that they showed a pleomorphism that increased with the degree of malignancy. The mean RMP's of glia from normal human and guinea pig cortex, human reactive cortex, and well differentiated astrocytomas were comparable, about −70 mV. In the less differentiated gliomas, the mean RMP's were lower, with the glioblastoma multiforme having the lowest value, −40 ± 7 mV. When the [K+]o was manipulated over a range of 2 to 40 mM/liter, the mean slope of RMP plotted against [K+]o indicated that normal human and guinea pig glia were exclusively permeable to K+ between [K+]o of 4 to 40 mM/liter. In contrast, the mean slope of reactive glia at these [K+]o's was less, suggesting a permeability to one or more additional ions. Below 4 mM/liter, the slopes of both normal and reactive glia showed changes in RMP smaller than the values expected of cells that are permeable only to K+. Like the reactive glia, the slopes derived for neoplastic cells did not indicate an exclusive permeability to K+, and some cells from the glioblastoma multiforme showed no change in RMP when [K+]o was varied.

Changes in [K+]o evoked by baclofen in guinea pig hippocampus

1998 ◽  
Vol 76 (2) ◽  
pp. 148-154 ◽  
Author(s):  
G V Obrocea ◽  
Mary E Morris
Keyword(s):  
Guinea Pig ◽  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
Brain Slices ◽  
Field Potential ◽  
Stratum Radiatum ◽  
Extracellular Potassium ◽  
Receptor Subtype ◽  
Field Potentials ◽  
Stratum Pyramidale

K+-sensitive microelectrodes were used to record changes evoked by baclofen in extracellular potassium concentration ([K+]o) and field potentials in the stratum pyramidale (SP) and stratum radiatum (SR) in the CA1b region of guinea pig hippocampal slices in vitro. Bath applications of ( ±)-baclofen (1 µM - 3 mM for approx 5 min) evoked changes in [K+]o, which were in most cases sustained throughout agonist application and reversed during washout. The maximal (Rmax) values for curves fitted to the concentration-response data were for SP and SR, respectively, 0.59 ± 0.03 and 0.65 ± 0.03 mM, and EC50 values were 39.7 and 39.4 µM, respectively. The evoked K+ and field potential changes were significantly correlated and could be blocked by 2-OH-saclofen (50 µM) and CGP 35348 (50 µM). In <= 10% of experiments baclofen (10-50 µM) induced either a decrease or a transient increase ( <= 1 min duration) in [K+]o; in some slices with concentrations >=20 µM an initial decrease preceded a progressive increase. Pressure ejection of baclofen (100 µM for 100-900 ms) evoked increases in [K+]o and field potentials, which were larger in SR than in SP. In <= 10% of slices brief and (or) sustained application of baclofen (by either bath perfusion or pressure ejection) also evoked synchronous, repetitive interictal and ictal discharges at frequencies approx 1/s and 1/12 s, respectively, an observation that affirms a proconvulsant capacity. It is concluded that (i) although increases in [K+]o evoked by baclofen in SR compared with SP are slightly larger, they are not significantly different, (ii) GABAB receptor subtype(s) in SR and SP appear similar, as they have identical affinities, and (iii) [K+]o accumulations evoked by GABA likely include a contribution from a GABAB receptor activated K+ conductance, especially in dendritic regions.Key words: brain slices, stratum pyramidale, stratum radiatum, GABAB receptors, ion-selective microelectrodes, epileptiform activity.

scholarly journals IMMUNE LYSIS OF NORMAL HUMAN AND PAROXYSMAL NOCTURNAL HEMOGLOBINURIA (PNH) RED BLOOD CELLS

1966 ◽  
Vol 123 (6) ◽  
pp. 969-984 ◽  
Author(s):  
Wendell F. Rosse ◽  
Robert Dourmashkin ◽  
John H. Humphrey
Keyword(s):  
Guinea Pig ◽  
Normal Serum ◽  
Red Cells ◽  
Human Complement ◽  
Minimum Number ◽  
Normal Human ◽  
Membrane Defects ◽  
The Mean ◽  
Complement Lysis ◽  
Human Red Cells

1. The defects produced on the membrane of the human red blood cell by the action of complement and antibody have been studied by the use of the electron microscope. These are round to slightly ovoid holes and are surrounded by an irregular ring, about 20 A thick. The mean diameter of the holes is about 103 A if human complement is used (regardless of the antibody used for sensitization) and about 88 A if guinea pig complement is used. 2. The holes in normal and PNH red cells appear to be identical, under the same conditions. The membrane defects produced by lysis of PNH cells with acidified normal serum (the Ham's test) are identical to those produced by complement lysis with specific antibody, indicating that complement is undoubtedly the cause of such lysis. 3. Evidence is presented that when human complement acts on human red cells sensitized with anti-I antibody, each complete activation of complement leads to the production of a cluster of holes. This contrasts to the action of guinea pig complement, on sheep cells, each activation of which leads to a single hole. 4. The maximum number of anti-I antibody molecules which can attach to a human red cell (i.e. the minimum number of antigen sites) is about 500,000 for both normal and PNH cells. 5. The number of holes produced during lysis of the PNH cell is the same as that of the normal cell. When all cells are lysed by am excess of C', a mean of about 90,000 holes are present on each membrane. When complement is limited, a larger proportion of PNH cells are lysed due to their peculiar sensitivity to C' but the number of holes on each lysed cell is the same as for normal cells lysed by the same concentration of C'.

Monoamine Oxidase and Other Mitochondrial Enzymes in Density Subpopulations of Human Platelets

1988 ◽  
Vol 59 (01) ◽  
pp. 029-033 ◽  
Author(s):  
K G Chamberlain ◽  
D G Penington
Keyword(s):  
Monoamine Oxidase ◽  
Protein Concentration ◽  
Close Correlation ◽  
Human Platelets ◽  
Mitochondrial Enzymes ◽  
Density Fractions ◽  
Percoll Gradients ◽  
Normal Human ◽  
The Mean ◽  
Very High

SummaryNormal human platelets have been separated according to density on continuous Percoll gradients and the platelet distribution divided into five fractions containing approximately equal numbers of platelets. The mean volumes and protein contents of the platelets in each fraction were found to correlate positively with density while the protein concentration did not differ significantly between the fractions. Four mitochondrial enzymes (monoamine oxidase, glutamate dehydrogenase, cytochrome oxidase and NADP-dependent isocitrate dehydrogenase) were assayed and their activities per unit volume were found to increase in a very similar monotonie fashion with platelet density. When MAO and GDH were assayed on the same set of density fractions the correlation between the two activities was very high (r = 0.94–1.00, p <0.001) and a similar close correlation was found between MAO and ICDH. The results support the hypothesis that high density platelets either have a higher concentration of mitochondria or have larger mitochondria than low density platelets.

scholarly journals Oxytocin Modulation of Maternal Behavior and Its Association With Immunological Activity in Rats With Cesarean Delivery

ASN NEURO ◽  
2021 ◽  
Vol 13 ◽  
pp. 175909142110147
Author(s):  
Tong Li ◽  
Shu-Wei Jia ◽  
Dan Hou ◽  
Xiaoran Wang ◽  
Dongyang Li ◽  
...  
Keyword(s):  
Cesarean Delivery ◽  
Maternal Behavior ◽  
Inflammatory Cytokine ◽  
Adrenocorticotropic Hormone ◽  
Brain Slices ◽  
Relative Weight ◽  
Resting Membrane Potential ◽  
Cytokine Release ◽  
Immunological Activity ◽  
Fos Expression

Oxytocin (OT), a neuropeptide produced in the supraoptic (SON) and paraventricular (PVN) nuclei, is not only essential for lactation and maternal behavior but also for normal immunological activity. However, mechanisms underlying OT regulation of maternal behavior and its association with immunity around parturition, particularly under mental and physical stress, remain unclear. Here, we observed effects of OT on maternal behavior in association with immunological activity in rats after cesarean delivery (CD), a model of reproductive stress. CD significantly reduced maternal interests to the pups throughout postpartum day 1-8. On postpartum day 5, CD decreased plasma OT levels and thymic index but increased vasopressin, interleukin (IL)-1β, IL-6 and IL-10 levels. CD had no significant effect on plasma adrenocorticotropic hormone and corticosterone levels. In the hypothalamus, CD decreased corticotropin-releasing hormone contents in the PVN but increased OT contents in the PVN and SON and OT release from hypothalamic implants. CD also increased c-Fos expression, particularly in the cytoplasm of OT neurons. Lastly, CD depolarized resting membrane potential and increased spike width while increasing the variability of the firing rate of OT neurons in brain slices. Thus, CD can increase hypothalamic OT contents and release but reduce pituitary release of OT into the blood, which is associated with depressive-like maternal behavior, increased inflammatory cytokine release and decreased relative weight of the thymus.

Cell loss from human, canine and guinea-pig gastric mucosa measured by DNA radioimmunoassay

1984 ◽  
Vol 66 (6) ◽  
pp. 701-708 ◽  
Author(s):  
B. C. Hurst ◽  
W. D. W. Rees ◽  
A. Garner
Keyword(s):  
Guinea Pig ◽  
Animal Species ◽  
Colorimetric Assay ◽  
Cell Loss ◽  
Mucosal Cell ◽  
Normal Human ◽  
Dna Loss ◽  
Guinea Pig Stomach ◽  
Pavlov Pouch ◽  
Stimulation Of

1. A DNA radioimmunoassay, sensitive in the range 25–1000 ng, has been developed to measure gastric mucosal cell loss. Validity of the assay was based on antibody specificity, absence of interference from gastric contents, parallel tracer displacement by dilutions of gastric and standard DNA, and crossover with colorimetric assay. 2. With this assay, gastric DNA shedding was examined in two animal species and man. In the guinea-pig stomach, DNA loss was 20–100 pg/h and in the canine Pavlov pouch, 260–580pg/h. In the canine Pavlov pouch stimulation of acid secretion by histamine and exposure to exogenous acid increased DNA output. In the normal human stomach DNA loss was 544 k 175 pg/h and in duodenal ulcer patients, 649 k 225 pg/li. 3. DNA radioimmunoassay provides a sensitive and reproducible measure of cell exfoliation from the stomach and may be a useful tool for studying aspects of gastric mucosal defence.

Calcium channels and excitation–contraction coupling in cardiac cells. I. Two components of contraction in guinea-pig papillary muscle

1987 ◽  
Vol 65 (9) ◽  
pp. 1821-1831 ◽  
Author(s):  
E. Honoré ◽  
M. M. Adamantidis ◽  
B. A. Dupuis ◽  
C. E. Challice ◽  
P. Guilbault
Keyword(s):  
Membrane Potential ◽  
Guinea Pig ◽  
Papillary Muscle ◽  
Cardiac Cells ◽  
Resting Membrane Potential ◽  
Tonic Component ◽  
Contraction Coupling ◽  
Rich Solution ◽  
The Relationship ◽  
Guinea Pig Atria

Biphasic contractions have been obtained in guinea-pig papillary muscle by inducing partial depolarization in K+-rich solution (17 mM) containing 0.3 μM isoproterenol; whereas in guinea-pig atria, the same conditions led to monophasic contractions corresponding to the first component of contraction in papillary muscle. The relationships between the amplitude of the two components of the biphasic contraction and the resting membrane potential were sigmoidal curves. The first component of contraction was inactivated for membrane potentials less positive than those for the second component. In Na+-low solution (25 mM), biphasic contraction became monophasic subsequent to the loss of the second component, but tetraethylammonium unmasked the second component of contraction. The relationship between the amplitude of the first component of contraction and the logarithm of extracellular Ca2+ concentration was complex, whereas for the second component it was linear. When Ca2+ ions were replaced by Sr2+ ions, only the second component of contraction was observed. It is suggested that the first component of contraction may be triggered by a Ca2+ release from sarcoplasmic reticulum, induced by the fast inward Ca2+ current and (or) by the depolarization. The second component of contraction may be due to a direct activation of contractile proteins by Ca2+ entering the cell along with the slow inward Ca2+ current and diffusing through the sarcoplasm. These results do not exclude the existence of a third "tonic" component, which could possibly be mixed with the second component of contraction.

scholarly journals Involvement of A pertussis Toxin Sensitive G-Protein in the Inhibition of Inwardly Rectifying K+Currents by Platelet-Activating Factor in Guinea-Pig Atrial Cardiomyocytes

1994 ◽  
Vol 3 (1) ◽  
pp. 45-51
Author(s):  
M. Gollasch ◽  
T. Kleppisch ◽  
D. Krautwurst ◽  
D. Lewinsohn ◽  
J. Hescheler
Keyword(s):  
Cyclic Amp ◽  
Guinea Pig ◽  
G Protein ◽  
Pertussis Toxin ◽  
Platelet Activating Factor ◽  
Resting Membrane Potential ◽  
Patch Clamp Technique ◽  
Guinea Pig Heart ◽  
Ventricular Cells ◽  
Inwardly Rectifying

Platelet-activating factor (PAF) inhibits single inwardly rectifying K+channels in guinea-pig ventricular cells. There is currently little information as to the mechanism by which these channels are modulated. The effect of PAF on quasi steady-state inwardly rectifying K+currents (presumably of the IK1type) of auricular, atrial and ventricular cardiomyocytes from guinea-pig were studied. Applying the patch-clamp technique in the whole-cell configuration, PAF (10 nM) reduced the K+currents in all three cell types. The inhibitory effect of PAF occurred within seconds and was reversible upon wash-out. It was almost completely abolished by the PAF receptor antagonist BN 50730. Intracellular infusion of atrial cells with guanine 5′-(β-thio)diphosphate (GDPS) or pretreatment of cells with pertussis toxin abolished the PAF dependent reduction of the currents. Neither extracellularly applied isoproterenol nor intracellularly applied adenosine 3′,5′-cyclic monophosphate (cyclic AMP) attenuated the PAF effect. In multicellular preparations of auricles, PAF (10 nM) induced arrhythmias. The arrhythmogenic activity was also reduced by BN 50730. The data indicate that activated PAF receptors inhibit inwardly rectifying K+currents via a pertussis toxin sensitive G-protein without involvement of a cyclic AMP-dependent step. Since IK1is a major component in stabilizing the resting membrane potential, the observed inhibition of this type of channel could play an important role in PAF dependent arrhythmogenesis in guinea-pig heart.

Comparison of changes evoked by GABA (γ-aminobutyric acid) and anoxia in [K+]o, [Cl-]o, and [Na+]o in stratum pyramidale and stratum radiatum of the guinea pig hippocampus

2000 ◽  
Vol 78 (5) ◽  
pp. 378-391 ◽  
Author(s):  
G V Obrocea ◽  
M E Morris
Keyword(s):  
Guinea Pig ◽  
Extracellular Space ◽  
Hippocampal Slices ◽  
Brain Slices ◽  
Receptor Activation ◽  
Ion Concentration ◽  
Aminobutyric Acid ◽  
Stratum Radiatum ◽  
Bicuculline Methiodide ◽  
Stratum Pyramidale

Ion-selective microelectrode recordings were made to assess a possible contribution of extracellular γ-aminobutyric acid (GABA) accumulation to early responses evoked in the brain by anoxia and ischemia. Changes evoked by GABA or N2 in [K+]o, [Cl-]o, [Na+]o, and [TMA+]o were recorded in the cell body and dendritic regions of the stratum pyramidale (SP) and stratum radiatum (SR), respectively, of pyramidal neurons in CA1 of guinea pig hippocampal slices. Bath application of GABA (1-10 mM) for approximately 5 min evoked changes in [K+]o and [Cl-]o with respective EC50 levels of 3.8 and 4.1 mM in SP, and 4.7 and 5.6 mM in SR. In SP 5 mM GABA reversibly increased [K+]o and [Cl-]o and decreased [Na+]o; replacement of 95% O2 -5% CO2 by 95% N2 -5% CO2 for a similar period of time evoked changes which were for each ion in the same direction as those with GABA. In SR both GABA and N2 caused increases in [K+]o and decreases in [Cl-]o and [Na+]o. The reduction of extracellular space, estimated from levels of [TMA+]o during exposures to GABA and N2, was 5-6% and insufficient to cause the observed changes in ion concentration. Ion changes induced by GABA and N2 were reversibly attenuated by the GABAA receptor antagonist bicuculline methiodide (BMI, 100 µM). GABA-evoked changes in [K+]o in SP and SR and [Cl-]o in SP were depressed by >=90%, and of [Cl-]o in SR by 50%; N2-evoked changes in [K+]o in SP and SR were decreased by 70% and those of [Cl-]o by 50%. BMI blocked Δ [Na+]o with both GABA and N2 by 20-30%. It is concluded that during early anoxia: (i) accumulation of GABA and activation of GABAA receptors may contribute to the ion changes and play a significant role, and (ii) responses in the dendritic (SR) regions are greater than and (or) differ from those in the somal (SP) layers. A large component of the [K+]o increase may involve a GABA-evoked Ca2+-activated gk, secondary to [Ca2+]i increase. A major part of [Cl-]o changes may arise from GABA-induced gCl and glial efflux, with strong stimulation of active outward transport and anion exchange at SP, and inward Na+/K+/2Cl- co-transport at SR. Na+ influx is attributable mainly to Na+-dependent transmitter uptake, with only a small amount related to GABAA receptor activation. Although the release and (or) accumulation of GABA during anoxia might be viewed as potentially protectant, the ultimate role may more likely be an important contribution to toxicity and delayed neuronal death. Key words: brain slices, ion-selective microelectrodes, stratum pyramidale, stratum radiatum, bicuculline methiodide, extracellular space shrinkage.

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