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H Landahl

Publications and source records attributed to H Landahl.

5 recordsLinked to original sources
PubMed1983

Activation of acetylcholine receptors causes the partition of hydrophobic cations into postsynaptic membrane vesicles.

In the continued presence of cholinergic ligands, the acetylcholine receptor-channel complex (AChR) in postsynaptic membranes undergoes a sequence of conformational changes. On addition of the ligand, the receptor rapidly changes from a closed channel to an open channel conformation, then slowly changes to a nonconducting state termed desensitization. The lifetime of the open channel conformation and the rate of desensitization are both dependent on the magnitude of the membrane potential, suggesting that the ligand-induced conformational changes in AChR may involve the movement of electrical charges within the membrane. Measurements of charge redistribution in AChR-containing membranes following ligand binding have not been reported. Recently, measurements of changes in the membrane partition coefficient of hydrophobic ions have been used to detect electrostatic changes in both biological and model membranes. We report here that cholinergic ligands induce changes in the partition coefficient of the hydrophobic cation tetraphenylphosphonium (TPP) into AChR-enriched membranes. The extent and time course of these changes in TPP partition coefficient are accounted for in a kinetic model. We conclude that TPP movement is a monitor of a molecular event which may be associated with the slow component of AChR desensitization.

Animals↗
PubMed1980

Comparison of storage- and signal-limited models of pancreatic insulin secretion.

Kinetic patterns of glucose-stimulated insulin secretion from the in vitro perfused pancreas were used to test different types of secretion models of similar complexity. A storage-limited, two-compartment model, modified slightly from that previously, was compared with signal-limited models incorporating delta or feedback characteristics. Mathematical relationships for all models were fixed by single-step, dose-response experiments and models were compared in a series of glucose test patterns including steps, step restimulations, staircases, pulses, ramps, and ramp restimulations. The work quantifies previously unreported characteristics of hypersensitivity and low-glucose rest/restimulation behavior in the pancreas. All models simulated staircase and ramp experiments. The two-compartment model contains an inherent hypersensitivity factor required for repeated pulse-type experiments. However, the kinetics of hypersensitivity were too rapid to be simulated in all types of pulse and ramp/pulse experiments by the restricted refilling characteristics as written into this model. The signal-limited, delta-feedback model did not inherently produce potentiation, but required add-on modification that then more closely simulated some pulse and ramp/pulse experiments. This model simulated experimental negative spikes, whereas the storage-limited model would require additional complexity to do so. These and other results suggest that both storage- and signal-limited models, although currently insufficient, could be elaborated to simulate available data. Therefore, a choice between the two to describe the underlying physiological mechanism of multiphasic insulin secretion is premature. The alternate possibility that the secretion mechanism may be reflected by a combination of the two models is presented.

Animals↗