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J P Pooler

Publications and source records attributed to J P Pooler.

23 records · Page 2Linked to original sources
PubMed1976

Ultraviolet-induced alterations of beat rate and electrical properties of embryonic chick heart cell aggregates.

Embryonic heart cell aggregates were irradiated with ultraviolet light at wavelengths between 260 and 310 nm. Spontaneous beat rate was monitored with the aid of a closed-circuit TV camera and, in separate experiments, electrophysiological changes were assayed by intracellular recording. The characteristic response of 7-day aggregates was an increase in spontaneous beat rate to a maximum plateau level, followed by a rather abrupt cessation of beating. Intracellular recordings during irradiation showed a marked decline in the maximum rate of rise, overshoot, and repolarization phase of the action potential, and a significant change in threshold toward zero. The action spectrum for the termination of beating peaked between 290 and 295 nm; it fell off sharply at longer wavelengths and more slowly at shorter wavelengths. The maximum increase in beat rate was increasingly greater for shorter wavelengths and exhibited no peak in the wavelength range investigated. The sensitivity of aggregates to 295-nm light, as measured by the inverse of irradiation time required to terminate beating, decreased with increasing aggregate size and external potassium concentration, was relatively independent of temperature, and increased with embryonic age. The ultraviolet-induced increase in beat rate and termination of beating are attributed to separate complementary processes, a depolarization of the membrane, and a decline in "fast" sodium conductance.

Action Potentials↗
PubMed1975

Ultraviolet photoalteration of ion channels in voltage-clamped lobster giant axons.

An analysis of the ultraviolet light-induced changes in ionic conductances of lobster giant axon membranes has been carried out using the double sucrose gap voltage-clamp technique. The predominant effect of monochromatic light from a xenon arc source in the 255 to 305 nm region is an irreversible reduction in the magnitude of sodium conductance, without change in sodium channel activation or inactivation kinetics. A considerably smaller reduction in the magnitude of potassium conductance occurs, with some slowing of potassium channel activation kinetics. Leakage conductance is essentially not altered. The fall in sodium conductance follows an exponential time course toward a zero asymptote. The rate constant for conductance decrease was used as an assay for the wavelength dependence. The sodium conductance was maximally sensitive at 290 nm. It is suggested that individual sodium channels are closed upon absorption of single photons by aromatic amino acid residues in membrane proteins.

Action Potentials↗
PubMed1975

Selective modification of sodium channel gating in lobster axons by 2, 4, 6-trinitrophenol: Evidence for two inactivation mechanisms.

Trinitrophernol (TNP) selectively alters the sodium conductance system of lobster giant axons as measured in current clamp and voltage clamp experiments using the double sucrose gap technique. TNP has no measurable effect on potassium currents but reversibly prolongs the time-course of sodium currents during maintained depolarizations over the full voltage range of observable currents. Action potential durations are increased also. Tm of the Hodgkin-Huxley model is not markedly altered during activation of the sodium conductance but is prolonged during removal of activation by repolarization, as observed in sodium tail experiments. The sodium inactivation versus voltage curve is shifted in the hyperpolarizing direction as is the inactivation time constant curve, measured with conditioning voltage steps. This shift speeds the kinetics of inactivation over part of the same voltage range in which sodium currents are prolonged, a contradiction incompatible with the Hodgkin-Huxley model. These results are interpreted as support for a hypothesis of two inactivation processes, one proceeding directly from the resting state and the other coupled to the active state of sodium conductance.

Action Potentials↗
PubMedDate not supplied

Dye-sensitized photodynamic inactivation of cells.

Living cells may be modified in diverse ways by the combined action of visible light and photosensitizing molecules. The effects appear most frequently as disruptions of subcellular structure, changes in surface membrane function or inhibition of mitotic ability. This review concentrates on the four most thoroughly studied cell types--yeast cells, nerve cells, erythrocytes, and cultured tumor cells. Research on these cells indicates that potency of sensitization depends at least as much on the factors affecting an association between sensitizer and cell prior to illumination as on photochemical properties. While sensitizers which permeate may lead to altered DNA, it appears that surface membrane modification occurs simultaneously and may be critical in the inactivation mechanism. There is much circumstantial evidence suggesting that excited singlet molecular oxygen acts as an intermediate between photoexcited sensitizer and target alteration. Proteins, lipids, and nucleic acids are all susceptible to photosensitized attack, but the correlation between cellular and molecular modification remains ill-defined. The use of the photodynamic process as a therapeutic technique, particularly in the treatment of malignant tumors, holds great promise, but awaits further research to develop greater selectivity of action.

Cell Survival↗