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001 ocm11979993;

003 OCoLC;

005 20250120151954.0;

008 850430s1985 xx af bm 000 0 eng d;

035 a| (Sirsi) o11979993;

035 a| (OCoLC)11979993;

049 a| EREE;

050 4 a| QL931b| .O77x 1985;

100 1 a| Orr, Liston A.q| (Liston Anderson),e| author.?| UNAUTHORIZED;

245 14 a| The ionic basis for elongated action potentials induced in nerve by tungsten-platinum metal /c| by Liston A. Orr.;

246 1 i| Abstract title:a| Ionic basis for elongated action potentials induced in nerve by platinized-tungsten metal;

264 0 c| 1985.;

300 a| 57 leaves, 8 unnumbered leaves of plates :b| illustrations ;c| 28 cm;

336 a| textb| txt2| rdacontent;

337 a| unmediatedb| n2| rdamedia;

338 a| volumeb| nc2| rdacarrier;

502 b| M.S.c| East Carolina Universityd| 1985;

500 a| "Presented to the faculty of the Department of Biology ... in partial fulfillment of the requirements for the degree Master of Science in Biology.";

500 a| Advisor: Gerhard W. Kalmus;

520 3 a| Crayfish giant axons were studied using axial wire, space and current clamp techniques. Following cannulation of an axon with a platinized-tungsten wire electrode both propagated and space-clamped action potentials (AP) elongated. AP duration was typically 200-300 mSec (maximum to 4 secs.) A slight slowing of the AP rise was noted. The process was reversible upon removal of the electrode from the axon. The effect was not dependent on the passing of current through the platinized-tungsten metal nor on any component of the platinizing solution. Neither pure tungsten or platinum nor platinized-platinum electrodes were effective. Membrane resistance (Rm) during the AP plateau was 50-300% higher than Rm at rest. The steady state I-V plot of the altered axon exhibited anomalous rectification for depolarizing steps. In the absence of an inward sodium current (TTX or low external Na⁺), anomalous rectification was abolished, while an inhibition of normal rectification remained. Ca⁺⁺ channel blockers verapamil and La³⁺ as well as Low Ca⁺⁺ were antagonistic to plateau formation. It is concluded that a product of the platinum-tungsten:axoplasm interaction produced elongated AP's by altering the membrane by: 1) block of normal K⁺ outward rectifying current; 2) decrease of steady-state outward K⁺ current; and 3) accentuation of an inward Ca⁺⁺ current during AP generation.;

504 a| Includes bibliographical references (leaves 53-57).;

650 0 a| Axons.=| ^A15055;

650 0 a| Action potentials (Electrophysiology)=| ^A6552;

650 2 a| Axons0| (DNLM)D001369=| ^A923045;

650 2 a| Action Potentials.0| (DNLM)D000200=| ^A1057991;

655 2 a| Academic Dissertation.0| (DNLM)D019478?| UNAUTHORIZED;

650 7 a| Action potentials (Electrophysiology)2| fast0| (OCoLC)fst00796224;

650 7 a| Axons.2| fast0| (OCoLC)fst00824509;

655 7 a| Academic theses.2| fast0| (OCoLC)fst01726453;

655 7 a| Academic theses.2| lcgft;

655 7 a| Thèses et écrits académiques.2| rvmgf0| (CaQQLa)RVMGF-000001173;

700 1 a| Kalmus, Gerhard W.,e| degree supervisor.?| UNAUTHORIZED;

710 2 a| East Carolina University.b| Department of Biology.=| ^A637467;

856 41 z| Access via ScholarShipu| http://hdl.handle.net/10342/11353;

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949 a| Click on web addressw| asish| hsl111;

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The ionic basis for elongated action potentials induced in nerve by tungsten-platinum metal / by Liston A. Orr.

Author/creator	Orr, Liston A. author.
Other author	Kalmus, Gerhard W., degree supervisor.
Other author	East Carolina University. Department of Biology.
Format	Theses and dissertations
Production	1985.
Description	57 leaves, 8 unnumbered leaves of plates : illustrations ; 28 cm
Supplemental Content	Access via ScholarShip
Subjects	Axons. Action potentials (Electrophysiology) Axons Action Potentials.

Variant title	Abstract title: Ionic basis for elongated action potentials induced in nerve by platinized-tungsten metal
Summary	Crayfish giant axons were studied using axial wire, space and current clamp techniques. Following cannulation of an axon with a platinized-tungsten wire electrode both propagated and space-clamped action potentials (AP) elongated. AP duration was typically 200-300 mSec (maximum to 4 secs.) A slight slowing of the AP rise was noted. The process was reversible upon removal of the electrode from the axon. The effect was not dependent on the passing of current through the platinized-tungsten metal nor on any component of the platinizing solution. Neither pure tungsten or platinum nor platinized-platinum electrodes were effective. Membrane resistance (Rm) during the AP plateau was 50-300% higher than Rm at rest. The steady state I-V plot of the altered axon exhibited anomalous rectification for depolarizing steps. In the absence of an inward sodium current (TTX or low external Na⁺), anomalous rectification was abolished, while an inhibition of normal rectification remained. Ca⁺⁺ channel blockers verapamil and La³⁺ as well as Low Ca⁺⁺ were antagonistic to plateau formation. It is concluded that a product of the platinum-tungsten:axoplasm interaction produced elongated AP's by altering the membrane by: 1) block of normal K⁺ outward rectifying current; 2) decrease of steady-state outward K⁺ current; and 3) accentuation of an inward Ca⁺⁺ current during AP generation.
General note	"Presented to the faculty of the Department of Biology ... in partial fulfillment of the requirements for the degree Master of Science in Biology."
General note	Advisor: Gerhard W. Kalmus
Dissertation note	M.S. East Carolina University 1985
Bibliography note	Includes bibliographical references (leaves 53-57).
Genre/form	Academic theses.
Genre/form	Academic theses.
Genre/form	Thèses et écrits académiques.

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The ionic basis for elongated action potentials induced in nerve by tungsten-platinum metal / by Liston A. Orr.

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