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Biomedical subjects

A Hermann

Publications and source records attributed to A Hermann.

At least 109 records · Page 6Linked to original sources
PubMed1987

Action and location of neuropeptide tyrosine (Y) on hippocampal neurons of the rat in slice preparations.

The action of bath applied NPY (1-1,000 nM) was investigated on hippocampal slices of the rat with extra- and intracellular recording. Neuropeptide Y (NPY) at 10-1,000 nM caused a concentration-dependent, long-lasting reduction of excitatory postsynaptic potentials (EPSPs) in the hippocampal subfield CA1 and the area dentata, and an even stronger reduction of population spikes. Paired pulse experiments with low intensity, stimulation-evoked PSPs showed a marked increase in facilitation in the presence of NPY, indicating a presynaptic action. Spontaneous burst firing of CA1 pyramidal cells in low calcium, high magnesium medium was reduced, indicating a partially postsynaptic inhibitory action of NPY on their dendrites. Intracellular recording from CA1 somata during NPY administration revealed a reduction of the amplitudes of excitatory-inhibitory postsynaptic potential (EPSP-IPSP) sequences in the absence of changes in membrane potential and conductance. Accommodation of firing during long depolarizing pulses and afterhyperpolarizations were unchanged. The innervation pattern of NPY immunoreactive fibers in the same regions was studied in slices adjacent to the ones used for electrophysiology by using antisera against NPY and light and electron microscopy. There is a dense innervation of CA1 by NPY-immunoreactive axons and terminals, particularly in the stratum moleculare. NPY-immunoreactive neurons are present in the stratum oriens and pyramidale. The NPY labeled axons of the stratum moleculare participate in numerous synaptic contacts with the smaller dendritic elements in this layer, many of which belong to pyramidal neurons. These observations provide evidence for a dendritic NPY-immunoreactive innervation of CA1 neurons, which is in keeping with the electrophysiological effects of NPY on pyramidal neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Fluctuations of the Ca2+-activated K+ current in Aplysia neurones.

Fluctuations of the Ca2+-activated K+ current were measured in identified Aplysia neurones under voltage clamp conditions. The amplitude of IK,Ca was manipulated by ionophoretic injections of Ca2+. At small amplitudes of Ca2+-activated outward currents the variance of the Ca2+-activated current fluctuations increases linearly with the mean outward current. The single-channel conductance estimated from the variance of the fluctuations and the mean outward current is 11 +/- 3 pS at -30 mV. Power spectra of the Ca2+-activated K+ current can be fitted by the sum of two Lorentzian components with corner frequencies of about 10 Hz and 120 Hz.

Animals↗
PubMed1987

Charybdotoxin selectively blocks small Ca-activated K channels in Aplysia neurons.

The action of charybdotoxin (ChTX), a peptide component isolated from the venom of the scorpion Leiurus quinquestriatus, was investigated on membrane currents of identified neurons from the marine mollusk, Aplysia californica. Macroscopic current recordings showed that the external application of ChTX blocks the Ca-activated K current in a dose- and voltage-dependent manner. The apparent dissociation constant is 30 nM at V = -30 mV and increases e-fold for a +50- to +70-mV change in membrane potential, which indicates that the toxin molecule is sensitive to approximately 35% of the transmembrane electric field. The toxin is bound to the receptor with a 1:1 stoichiometry and its effect is reversible after washout. The toxin also suppresses the membrane leakage conductance and a resting K conductance activated by internal Ca ions. The toxin has no significant effect on the inward Na or Ca currents, the transient K current, or the delayed rectifier K current. Records from Ca-activated K channels revealed a single channel conductance of 35 +/- 5 pS at V = 0 mV in asymmetrical K solution. The channel open probability increased with the internal Ca concentration and with membrane voltage. The K channels were blocked by submillimolar concentrations of tetraethylammonium ions and by nanomolar concentrations of ChTX, but were not blocked by 4-aminopyridine if applied externally on outside-out patches. From the effects of ChTX on K current and on bursting pacemaker activity, it is concluded that the termination of bursts is in part controlled by a Ca-activated K conductance.

Action Potentials↗
PubMed1986

Source localization in intracavitary 60Co therapy with semiconductor and TL detectors.

Thermoluminescence and p-type semiconductor detectors were used for localization of the source in intracavitary (modified Stockholm method) treatment. The results were compared with X-ray films, and especially good agreement was obtained if the detectors were positioned on both sides of the patients. The measurements performed on Stage III to IV carcinoma cervix uteri patients indicate that the intracavitary source can deviate to both sides with equal probability. The magnitude of the deviation is described by a Gaussian distribution with an expected value of zero and S.D. of 8mm.

Brachytherapy↗
PubMed1985

Effects of caffeine on hippocampal pyramidal cells in vitro.

The effects of caffeine on the electrophysiological properties of CA1 pyramidal neurones were investigated in the rat hippocampal slice preparation in vitro. A concentration-dependent increase in both the extracellularly recorded excitatory postsynaptic potential (e.p.s.p.) and the population spike resulting from stimulation of the stratum radiatum could be evoked by caffeine with a threshold concentration of 10 microM. Intracellular recordings demonstrate a caffeine-evoked decrease in resting membrane potential, an increase in input resistance, a reduction of the long afterhyperpolarization (a.h.p.) and a decrease in accommodation. The interaction between caffeine and adenosine was investigated on the extracellularly recorded e.p.s.p. The maximal response evoked by caffeine was increased in the presence of adenosine and the adenosine concentration-response curve was shifted to the right in a parallel fashion in the presence of caffeine. It is suggested that the effects of caffeine on hippocampal neurones may be mediated by a decrease of one or more potassium conductance(s), and that adenosine and caffeine may compete for the same electrophysiologically active receptor site on these cells.

Adenosine↗
PubMed1984

Asymmetric lipid fluidity in human erythrocyte membrane: new spin-label evidence.

We have synthesized spin-labeled analogues of phosphatidylcholine, phosphatidylserine, and phosphatidylethanolamine with a short beta chain (C5) bearing a doxyl group at the fourth position. When added to an erythrocyte suspension, the labels immediately incorporate in the membrane. The orientation of the spin-labels was assessed in the bilayer (i) by addition in the medium of a nonpermeant reducer (ascorbate at 5 degrees C) or (ii) by following spontaneous reduction at 37 degrees C due to the endogenous reducing agents present in the cytosol. Both techniques prove that the spin-labels are originally incorporated in the outer leaflet and redistribute differently after incubation. After a 5-h incubation at 5 degrees C, the phosphatidylcholine derivative remained in the outer layer, while the phosphatidylethanolamine and phosphatidylserine derivatives were found principally in the inner leaflet. During the incubation, a small fraction of the spin-labels is hydrolyzed, particularly the phosphatidylserine derivative, presumably by an endogenous phospholipase A2. Because the hydrolyzed spin-labeled fatty acids are rejected in the aqueous phase, the spectra of the intact membrane-bound phospholipids can be obtained by an adequate spectral subtraction. The ESR spectrum corresponding to a probe in the outer leaflet indicates a more restricted motion than that associated with probes in the inner leaflet. Additional experiments have been carried out to prove that the difference in viscosity, which is likely to be due to anisotropic cholesterol distribution, is not attributable to modification of the cell morphology.(ABSTRACT TRUNCATED AT 250 WORDS)

Electron Spin Resonance Spectroscopy↗
PubMed1984

Action of quinidine on ionic currents of molluscan pacemaker neurons.

The effects of quinidine on the fast, the delayed, and the Ca2+-activated K+ outward currents, as well as on Na+ and Ca2+ inward currents, were studied at the soma membrane from neurons of the marine mollusk Aplysia californica. External quinidine blocks these current components but to different degrees. Its main effect is on the voltage-dependent, delayed K+ current, and it resembles the block produced by quaternary ammonium ions (Armstrong, C. M., 1975, Membranes, Lipid Bilayers and Biological Membranes: Dynamic Properties, 3:325-358). The apparent dissociation constant is 28 microM at V = +20 mV. The blocking action is voltage and time dependent and increases during maintained depolarization. The data are consistent with the block occurring approximately 70-80% through the membrane electric field. Internal injection of quinidine has an effect similar to that obtained after external application, but its time course of action is faster. External quinidine may therefore have to pass into or through the membrane to reach a blocking site. The Ca2+-activated K+ current is blocked by external quinidine at concentrations 20-50-fold higher compared with the delayed outward K+ current. In addition, it prolongs the time course of decay of the Ca2+-activated K+ current. Na+ and Ca2+ inward currents are also blocked by external quinidine, but again at higher concentrations. The effects of quinidine on membrane currents can be seen from its effect on action potentials and the conversion of repetitive "beating" discharge activity to "bursting" pacemaker activity.

Animals↗
PubMed1983

Conversion of beating to bursting pacemaker activity: action of quinidine.

External quinidine converts the pacemaker neurone L-11, found in the Aplysia abdominal ganglion, from spontaneously "beating" to "bursting" discharge activity. Quinidine-induced bursting ceased when entry of Ca2+ ions into the cells was blocked in a Ca2+-free, Co2+-containing solution or if internal Ca2+ accumulation was prevented by the injection of EGTA. The analysis of membrane currents from voltage clamp experiments showed that quinidine blocks the Ca2+ inward current in a dose- and time-dependent manner. In addition, the currents were displaced to the left on the voltage axis, causing an increase of the inward current at negative membrane potentials. External quinidine suppresses the Ca2+-activated K+ current induced by intracellular Ca2+ injections and acts to prolong its decay phase. The slowing of the decay phase of the Ca2+-activated K+ current by quinidine was prevented after intracellular injection of EGTA, indicating that Ca2+ removal is impaired by the drug. It is suggested that the increase of Ca2+ inward current at negative potentials and the prolonged activation of the Ca2+-activated K+ current play a major role in causing the bursting discharge behavior in normally beating cells.

Animals↗
PubMed1983

A comparison of the effects of long-term alcohol abuse and aging on the performance of verbal and nonverbal divided attention tasks.

The purpose of this study was to assess two versions of the hypothesis that alcohol abuse results in premature aging of the brain and of cognitive functioning. The performances of detoxified long-term alcoholic was compared with that of nonalcoholic controls on three divided attention tasks known to be sensitive to aging. While both forms of the premature aging hypothesis predicted that alcoholics should perform more poorly than controls, the hypotheses differed in their predictions of the interactions between the effects of alcohol and normal aging. The results showed that while all three tasks were sensitive to age, only two were affected by long-term alcohol abuse. On one of the tests affected by both age and alcohol abuse, the performance of both young and old alcoholics was equally impaired whereas on the other, only the older alcoholics had significant difficulties. Based on these findings it was concluded that there was only partial overlap between the effects of alcohol and aging, and that neither of the two forms of the premature aging hypothesis could predict the observed pattern of results.

Aging↗
PubMed1983

Learning to associate names and faces. Impaired acquisition on an ecologically relevant memory task by male alcoholics.

The performance of a group of detoxified male chronic alcoholics was compared with that of age-matched nonalcoholic controls on a memory task which at face value seemed relevant to daily life--i.e., learning to associate people's names with their faces. The alcoholics not only made more errors while learning the face-name associations than did the controls, but fewer of them were able to reach the learning criterion. However, 1 hour later, the alcoholics were nevertheless able to recognize all of the faces and names used during acquisition. The savings scores for the alcoholics, an index of the relative number of face-name associations retained during the 1-hour interval, did not differ significantly from those of the controls. These results demonstrate that the alcoholics' paired-associate learning deficit on this ecologically relevant task is related to their failure to form associations rather than to deficiencies in recognition memory or perceptual processes.

Age Factors↗
PubMed1983

On the statistics of 32P enrichment in skin tumours.

The authors have determined the distribution of 32P in normal skin and in the case of certain skin tumours (basalioma and spinalioma). In both groups a lognormal distribution was found. It may be assumed that the enrichment is governed by similar distribution in the case of melanoma malignum.

Basal Cell Carcinoma↗
PubMed1982

[Endobronchial metastases of extrathoracic malignancies].

The importance of endobronchial metastases originating from extrathoracic malignant tumors is emphasized and illustrated with 11 personally observed cases and with 87 cases from the literature. The primary tumors most frequently found are carcinoma of the breast, hypernephroma, and carcinoma of colon and rectum. 7 of the authors' own 11 patients are still alive at the time of publication, including two women 24 and 12 months respectively after pulmonary resection for endobronchial metastasis from carcinoma of the rectum.

Adenocarcinoma↗
PubMed1982

Properties of a Ca2+ activated K+ conductance in Helix neurones investigated by intracellular Ca2+ ionophoresis.

1. Membrane current responses produced by intracellular ionophoretic injection of Ca2+ ions into voltage clamped Helix neurones were investigated. 2. The Ca2+ activated current depends on the intensity and duration of the Ca2+ injection as well as on the membrane potential. The current-voltage relation is non-linear and shows strong outward rectification. 3. The Ca2+ activated current reverses near the equilibrium potential for K+ ions and the associated current fluctuations disappear at the K+ reversal potential, which indicates a single current source, probably activation of K+ channels. 4. The Ca2+ activated K+ conductance is voltage dependent and changes e-fold per 31 mV membrane depolarization. 5. Extracellular tetraethylammonium, gallamine and quinidine block the Ca2+ activated K4 current. Extracellular 4-aminopyridine has no blocking effect. 6. Sustained injection of high amounts of Ca2+ irreversibly suppresses the outward current. 7. The K+ outward current evoked by repeated Ca2+ injection exhibits summation and facilitation.

Animals↗
PubMed1982

Ionic requirements for membrane oscillations and their dependence on the calcium concentration in a molluscan pace-maker neurone.

1. Membrane currents from the bursting pace-maker neurone R-15 of Aplysia were measured under conditions designed to simulate membrane oscillations. Changes in the absorbance of the Ca(2+)-sensitive dye arsenazo III were used to monitor changes in the free intracellular Ca(2+) concentration, [Ca](i), under these conditions. In addition, changes in the extracellular K(+), concentration [K](o) were measured with K(+)-sensitive electrodes.2. In normal external ionic conditions the depolarizing phase of pace-maker activity was associated with a slow inward current and the hyperpolarizing phase with a slow outward current.3. In cells where the early inward Na(+) current was blocked by tetrodotoxin and outward K(+) currents were suppressed by intracellular EGTA and extracellular tetraethylammonium and 4-aminopyridine, the slow inward current was significantly larger in amplitude and was suppressed by removal of external Ca(2+) or the addition of external La(3+), but not by the removal of external Na(+).4. The slow inward current was increased when [Ca](o) was raised and decreased when it was reduced in the manner expected for current flow through a Ca(2+) channel. The selectivity of the slow inward current for divalent cations was [Formula: see text].5. The slow inward current was only slightly reduced by a 10 degrees C reduction in temperature.6. In normal external and internal ionic conditions changes in dye absorbance occurred when the membrane was depolarized with slow triangular voltage ramps or long depolarizing steps within the pace-maker oscillation range. The obsorbance change, and thus the increase in Ca(2+), [Ca](i), was well correlated with the appearance of the slow inward current. Moreover, the magnitude of the slow outward current was dependent upon the change in [Ca](i).7. The slow inward current and a substantial fraction of the outward current, as well as the change in [Ca](i), were reduced appreciably by the addition of La(3+) ions (3 mM) to the external medium.8. The increase in [Ca](i) during prolonged depolarization was not affected by external tetrodotoxin or by the removal of external Na(+), but was abolished by a Ca(2+)-free external medium containing EGTA. Nevertheless, significant changes occurred in [Ca](i) during depolarization in 0.1 mM-external Ca(2+).9. In normal external and internal ionic conditions extracellular K(+), [K](o), increased during the depolarizing phase of the pace-maker cycle and decayed during the hyperpolarizing phase.10. There was a measurable increase in [K](o) during small prolonged depolarizing steps which produced a net inward current, indicating that inward and outward currents overlap under normal conditions.11. In the absence of action potential discharge, [Ca](i) increased during the depolarizing phase and decreased during the hyperpolarizing phase of the membrane oscillation.12. It is proposed that pace-maker oscillations depend upon three separate but linked systems which include a voltage-dependent Ca(2+) current, the free intracellular Ca(2+) concentration and the Ca(2+)-activated K(+) current.

Animals↗
PubMed1982

Quantitative differences in the currents of bursting and beating molluscan pace-maker neurones.

1. The spontaneous activity and the membrane conductances to Na(+), Ca(2+) and K(+) ions of the bursting pace-maker neurone R-15 and the repetitively discharging (beating) pace-maker neurone L-11 in the abdominal ganglion of the marine mollusc, Aplysia californica, were compared.2. The bursting pace-maker R-15 can be converted to a beating pace-maker neurone by the removal of external Ca(2+) or by the injection of EGTA intracellularly. Bursting pace-maker activity is not restored by changes in the resting potential.3. Spontaneous action potentials of cell R-15 are reduced, but not abolished, by the addition of tetrodotoxin (TTX) to block Na(+) currents or by the removal of external Ca(2+) to abolish Ca(2+) currents, whereas the spontaneous action potentials of cell L-11 are abolished by external TTX, but are unaffected by external Ca(2+) removal.4. The membranes of both cells contain Na(+) and Ca(2+) inward currents. The specific Na(+) conductance of both cells is of similar magnitude, whereas the specific Ca(2+) conductance is about half the Na(+) conductance in R-15 cells and an order of magnitude smaller in L-11 cells.5. The delayed K(+) conductance of cell L-11 is about 1.2 times greater than this conductance in cell R-15. The transient K(+) currents of the two cells are about the same magnitude.6. The Ca(2+)-activated K(+) conductance of cell R-15 and cell L-11 was estimated using two methods. The Ca(2+)-activated K(+) conductance of cell R-15 estimated from the difference in the total outward current in normal external solution and the delayed K(+) current in Ca(2+)-free solution (to preclude Ca(2+) influx) or after internal EGTA injection (to prevent Ca(2+) accumulation) is about 23 times greater than this conductance in cell L-11. The Ca(2+)-activated K(+) conductance of cell R-15, estimated from local internal Ca(2+) injections in Ca(2+)-free solution, is about 3 times greater than this conductance in cell L-11.7. The leakage conductance of cell L-11 is about 1.3 times greater than this conductance in cell R-15. This conductance increases by a factor of about 2 in both cells in Ca(2+)-free external solutions containing 1 mM-EGTA, but is unchanged or is decreased slightly by injection of EGTA internally.8. It is concluded that the Ca(2+) conductance and the Ca(2+)-activated K(+) conductance are appreciably greater in the bursting pace-maker neurone R-15 than in the beating pace-maker neurone L-11, whereas other voltage-dependent conductances to Na(+) and K(+) ions as well as the leakage conductance are quite similar. These quantitative differences provide a basis for understanding the different spontaneous activities of the two cells.

Action Potentials↗