The interaction of κ-bungarotoxin with the nicotinic receptor of bovine chromaffin cells

Whole-cell recording techniques were used to examine acetylcholine-induced nicotinic currents in isolated bovinei chromaffin cells. The effects on these currents of κ-bungarotoxin, a snake venon κ-neurotoxin, were tested. Exposure of cells to κ-bungarotoxin (600 nM for 40 min) produced a prolonged b...

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Veröffentlicht in:Brain research 1992-02, Vol.573 (1), p.77-82
Hauptverfasser: Nooney, Janet M., Lambert, Jeremy J., Chiappinelli, Vincent A.
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description Whole-cell recording techniques were used to examine acetylcholine-induced nicotinic currents in isolated bovinei chromaffin cells. The effects on these currents of κ-bungarotoxin, a snake venon κ-neurotoxin, were tested. Exposure of cells to κ-bungarotoxin (600 nM for 40 min) produced a prolonged blockade of nicotinic currents. The mechanism of this blockade was examined in several ways. Firstly, the pre-exposure of cells to trimetaphan, a competitive nicotinic antagonist, protected against the action of subsequent additions of κ-bungarotoxin. Secondly, voltage-clamp measurements indicated that the degree of blockade produced by κ-bungarotoxin was independent of cell membrane potential. Unlike (+)-tubocurarine, κ-bungarotoxin had no direct agonist effects on nicotinic receptors. It is concluded from the present functional studies and from previously reported binding studies that κ-bungarotoxin blocks nicotinic responses in bovine chromaffin cells by binding to regions overlying acetylcholine sites on nicotinic receptors.
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Psychology ; Ganglionic Stimulants - pharmacology ; Molecular and cellular biology ; Monoamines receptors (catecholamine, serotonine, histamine, acetylcholine) ; Nicotinic Antagonists ; Nicotinic receptor ; Trimethaphan - pharmacology ; κ-bungarotoxin</subject><ispartof>Brain research, 1992-02, Vol.573 (1), p.77-82</ispartof><rights>1992 Elsevier Science Publishers B.V. 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The effects on these currents of κ-bungarotoxin, a snake venon κ-neurotoxin, were tested. Exposure of cells to κ-bungarotoxin (600 nM for 40 min) produced a prolonged blockade of nicotinic currents. The mechanism of this blockade was examined in several ways. Firstly, the pre-exposure of cells to trimetaphan, a competitive nicotinic antagonist, protected against the action of subsequent additions of κ-bungarotoxin. Secondly, voltage-clamp measurements indicated that the degree of blockade produced by κ-bungarotoxin was independent of cell membrane potential. Unlike (+)-tubocurarine, κ-bungarotoxin had no direct agonist effects on nicotinic receptors. It is concluded from the present functional studies and from previously reported binding studies that κ-bungarotoxin blocks nicotinic responses in bovine chromaffin cells by binding to regions overlying acetylcholine sites on nicotinic receptors.</description><subject>Acetylcholine</subject><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bovine adrenomedullary chromaffin cell</subject><subject>Bungarotoxins - pharmacology</subject><subject>Cattle</subject><subject>Cell receptors</subject><subject>Cell structures and functions</subject><subject>Cells, Cultured</subject><subject>Enterochromaffin Cells - drug effects</subject><subject>Enterochromaffin Cells - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Ganglionic Stimulants - pharmacology</subject><subject>Molecular and cellular biology</subject><subject>Monoamines receptors (catecholamine, serotonine, histamine, acetylcholine)</subject><subject>Nicotinic Antagonists</subject><subject>Nicotinic receptor</subject><subject>Trimethaphan - pharmacology</subject><subject>κ-bungarotoxin</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEuOEzEQhi00KGQCNwCpFyM0LBpc_XJ7MxKKeEkjkUVYsLKq3WVilNgZ2xngahyCM-EmUWbHpkql-v5S6WPsOfDXwKF7wznvyl7K-lpWryQHaMvVIzaHXlRlVzX8gs3PyBN2GeP3PNa15DM2g1Z0bd3N2df1hgrrEgXUyXpXeFP8-V0OB_cNg0_-p3XFD5s2Rcqcs9onm2sRSNM--TDhg7-3jgq9CX6HxuSApu02PmWPDW4jPTv1Bfvy_t16-bG8_fzh0_LtbakbEKkUEjVHiaT7vhraGkRf0ViBMGLQxjQ9dlzzAYeGTN_2yIcRTS1HAbw1krBesJfHu_vg7w4Uk9rZOH2AjvwhKuggG2ghg80R1MHHGMiofbA7DL8UcDUZVZMuNelSslL_jKpVjr043T8MOxofQkeFeX912mPUuDUBnbbxjLUAnAuRsZsjRtnFvaWgorbkNI02y0xq9Pb_f_wFTkyUjQ</recordid><startdate>19920221</startdate><enddate>19920221</enddate><creator>Nooney, Janet M.</creator><creator>Lambert, Jeremy J.</creator><creator>Chiappinelli, Vincent A.</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope></search><sort><creationdate>19920221</creationdate><title>The interaction of κ-bungarotoxin with the nicotinic receptor of bovine chromaffin cells</title><author>Nooney, Janet M. ; Lambert, Jeremy J. ; Chiappinelli, Vincent A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-79ac0a9aec882b531782ed217f7bcff48a60c0bab4ef858a0bdaf39d7105f9ea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Acetylcholine</topic><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bovine adrenomedullary chromaffin cell</topic><topic>Bungarotoxins - pharmacology</topic><topic>Cattle</topic><topic>Cell receptors</topic><topic>Cell structures and functions</topic><topic>Cells, Cultured</topic><topic>Enterochromaffin Cells - drug effects</topic><topic>Enterochromaffin Cells - metabolism</topic><topic>Fundamental and applied biological sciences. 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The effects on these currents of κ-bungarotoxin, a snake venon κ-neurotoxin, were tested. Exposure of cells to κ-bungarotoxin (600 nM for 40 min) produced a prolonged blockade of nicotinic currents. The mechanism of this blockade was examined in several ways. Firstly, the pre-exposure of cells to trimetaphan, a competitive nicotinic antagonist, protected against the action of subsequent additions of κ-bungarotoxin. Secondly, voltage-clamp measurements indicated that the degree of blockade produced by κ-bungarotoxin was independent of cell membrane potential. Unlike (+)-tubocurarine, κ-bungarotoxin had no direct agonist effects on nicotinic receptors. 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subjects Acetylcholine
Acetylcholine - pharmacology
Animals
Biological and medical sciences
Bovine adrenomedullary chromaffin cell
Bungarotoxins - pharmacology
Cattle
Cell receptors
Cell structures and functions
Cells, Cultured
Enterochromaffin Cells - drug effects
Enterochromaffin Cells - metabolism
Fundamental and applied biological sciences. Psychology
Ganglionic Stimulants - pharmacology
Molecular and cellular biology
Monoamines receptors (catecholamine, serotonine, histamine, acetylcholine)
Nicotinic Antagonists
Nicotinic receptor
Trimethaphan - pharmacology
κ-bungarotoxin
title The interaction of κ-bungarotoxin with the nicotinic receptor of bovine chromaffin cells
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