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.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001369:Axons / Q000187:drug effects / Q000502:physiology*; D004229:Dithiothreitol / Q000494:pharmacology; D006821:Hyaluronoglucosaminidase; D008433:Mathematics; D008121:Nephropidae; D009439:Neuraminidase; D011402:Pronase; D013997:Time Factors; D014357:Trypsin
D009439:Neuraminidase; D006821:Hyaluronoglucosaminidase; D014357:Trypsin; D011402:Pronase; D004229:Dithiothreitol