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H Landolt

Publications and source records attributed to H Landolt.

46 records · Page 3Linked to original sources
PubMed1981

Effects of substance P on neurones and glial cells in cultured rat spinal cord.

Substance P caused a depolarization of cultured spinal neurones which was often accompanied by a decrease in membrane conductance. The peptide usually had no effect on the membrane potential and resistance of glial cells. In contrast to the depolarization by glutamate, which is associated with an influx of Na+ and an efflux of K+, the action of substance P may be due to a decrease of the K+-conductance.

Animals↗
PubMed1981

Efflux of potassium from neurones excited by glutamate and aspartate causes a depolarization of cultured glial cells.

The time course of the depolarization of cultured astrocytes and neurones by glutamate and aspartate corresponds well with the increase of the extracellular K+ concentration ([K +]0) measured with an ion-sensitive microelectrode placed in the close vicinity of the cells tested. It is concluded that the depolarization of glial cells is caused by an efflux of K+ from neighbouring neurones during their excitation by the amino acids.

Animals↗
PubMed1981

Evidence that the depolarization of glial cells by inhibitory amino acids is caused by an efflux of K+ from neurones.

The action of inhibitory amino acid transmitters GABA, glycine, beta-alanine and taurine has been studied on the membrane potential of cultured astrocytes and on the extracellular K+-concentration ([K+]0) using K+-sensitive microelectrodes. All four amino acids caused a depolarization of glial cells and an increase of [K+]0. The effects produced by GABA were usually more pronounced than those caused by the other amino acids. Simultaneous recordings of the action of GABA and glycine on the glial membrane potential and on [K+]0 usually revealed a good correlation in time course, but often there were differences between the amplitudes of glial depolarizations and the values calculated from the [K+]0 increase. 4-Aminopyridine, which blocks K+-conductance of excitable membranes, reversibly abolished both the glial depolarization and the [K+]0 increased produced by GABA and glycine. From these results it is concluded that unlike neurones, glial cells do not have receptors for these amino acid transmitters and that their action on glial cells is caused by the efflux of K+ from activated neurones.

Amino Acids↗
PubMed1981

GABA and glycine receptors in CNS cultures: autoradiographic binding and electrophysiological studies.

Autoradiographic studies have shown that GABA, glycine and their antagonists bicuculline and strychnine are bound to many cultured neurones but not to glial cells. The hyperpolarization of GABA and glycine on CNS neurones is associated with an increase in membrane conductance, whereas the depolarization of glial cells by these amino acids is not accompanied by a change in membrane resistance. Using K+-sensitive electrodes, it was observed that the glial depolarization correlates well with the increase of the extracellular K+-concentration. 4-AP which blocks K+-conductance of excitable cells reversibly abolished both the glial depolarization and the increase of extracellular K+-concentration caused by GABA and glycine. It is concluded that, unlike neurones, glial cells may not possess receptors for GABA and glycine and that the depolarization by these amino acids is an indirect effect caused by an increase of extracellular K+ released from adjacent neurones.

Animals↗
PubMedDate not supplied

Sleep estimation from wrist activity in patients with major depression.

Actigraphy has been used to monitor individuals' sleep and wakefulness patterns without laboratory confinement. To date, its validity in monitoring sleep and wakefulness among patients with major depressive episodes has not been systematically examined. The present study investigated whether the normative criteria of the Actigraph Data Analysis Software, initially optimized for healthy individuals, could score wrist-activity data accurately in a sample of depressed patients. Application of the normative algorithm yielded a correlation coefficient of 0.85 and an average error of 35 min, comparing actigraphic and polysomnographic sleep estimates. The algorithm optimized for this sample provided a correlation coefficient of 0.81 and an error of 6 minutes. For both algorithms, agreement for individual comparisons varied substantially. These findings suggest that scoring criteria optimized on wrist-activity data of healthy young adults may not produce optimal results for patients characterized with major depressive episodes.

Adult↗