QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by J. ASHFORD, M. L. Articles by R. USHERWOOD, P. N. Search for Related Content PubMed Articles by J. ASHFORD, M. L. Articles by R. USHERWOOD, P. N.

Journal of Experimental Biology 134,131-154 (1988)
Published by Company of Biologists 1988

Voltage-Dependent Block of Locust Muscle Glutamate Channels by Chlorisondamine

M. L. J. ASHFORD ¹, P. BODEN ², R. L. RAMSEY ³, M. S. P. SANSOM ³, H. SHINOZAKI ⁴, and P. N. R. USHERWOOD ³

¹ Department of Zoology, University of Nottingham University Park, Nottingham NG7 2RD; Department of Pharmacology, University of Cambridge, Hills Road, Cambridge
² Department of Zoology, University of Nottingham University Park, Nottingham NG7 2RD; Parke-Davis Research Unit, Addenbrooke's Hospital Site, Hills Road, Cambridge
³ Department of Zoology, University of Nottingham University Park, Nottingham NG7 2RD
⁴ Department of Zoology, University of Nottingham University Park, Nottingham NG7 2RD; Tokyo Metropolitan Institute of Medical Science, Bunkyo-Ku, Tokyo 113, Japan

Chlorisondamine reversibly reduced the amplitude of the neurally evoked twitch of locust retractor unguis muscle in a dose-dependent manner and also blocked agonist-induced contractions. Depolarizations elicited by ionophoresis of L-glutamate were also reduced in amplitude by chlorisondamine, but there was no effect of this drug on desensitization. Neurally evoked synaptic currents were reduced in amplitude, their rise time was decreased and their decay phase made biphasic (or more complex) by chlorisondamine (>10^-5 mol 1^-1). These effects of chlorisondamine were voltage-dependent, such that at very hyperpolarized potentials (-120 mV and -140 mV) there was an apparent reduction in the degree of block. Single-channel studies indicate that chlorisondamine acts to block the channel both in the open and the closed form and that these actions are dependent on concentration and voltage. The actions of chlorisondamine are discussed in relation to the basic kinetic models of channel block.

Key words: channel block, glutamate receptors, chlorisondamine, locust muscle

Accepted on August 26, 1987