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Biomedical subjects

M W Kaplan

Publications and source records attributed to M W Kaplan.

21 records · Page 2Linked to original sources
PubMed1977

Slow bleach-induced birefringence changes in rod outer segments.

1. Time resolved birefringence measurements reveal complex structural changes in rod outer segments following a bleaching flash. 2. The detailed character of the observed changes depends upon osmotic integrity of the outer segment envelope membrane. Rod outer segments with intact envelope membranes show a fast initial loss of intrinsic birefringence simultaneous with the formation of metarhodopsin II followed by a slower secondary loss. A subsequent birefringence increase to higher than the dark-adapted level is partially correlated with the formation of retinol. Rod outer segments with ruptured envelope membranes show the initial and secondary losses, but the subsequent recovery only reaches the dark-adapted level. Retinol does not form in such organelles. 3. The slow birefringence changes in intact rod outer segments were qualitatively different when Na+ salts were replaced by equimolar K+ salts in the bathing medium. 4. Glycerol appears to influence both the rate and magnitude of metarhodopsin III formation, and of the spectrally silent secondary birefringence loss.

Animals↗
PubMed1975

Modification of optical responses associated with the action potential of lobster giant axons.

The sources of optical retardation changes and light scattering changes occurring during the action potential propagation of lobster giant axons have been investigated. A technique has been developed for resolving the total transmitted-light intensity change into a retardation change component, dI-r, and a forward direction light scattering change, dI-s. Trypsin, pronase, neuraminidase and hyaluronidase all reduce the magnitude of dI-r without diminishing the action potential, probably by cleaving charged saccharides. Dithiothreitol has no effect. This suggests that glycoproteins and hyaluronic acid polymers at the surface of the axon are involved in the optical responses, either by being passively realigned or by contributing to compression and expansion forces as the membrane electric field changes. Large dI-s responses are generated by trypsin and pronase treatment. The modifying effects of these proteases may be due to modification of the membrane or to increases in the refractive index of the medium surrounding the axon, since similar large dI-s, responses are produced by increasing the refractive index with sucrose. Since large reductions in dIr can be produced without concurrent reductions in the action potential, a significant portion of the optical retardation responses cannot be attributable to structural changes that are causally related to membrane ionic permeability changes during the action potential.

Action Potentials↗