PT  - JOURNAL ARTICLE
AU  - M Bertolino
AU  - S Vicini
TI  - Voltage-dependent block by strychnine of N-methyl-D-aspartic acid-activated cationic channels in rat cortical neurons in culture.
DP  - 1988 Aug 01
TA  - Molecular Pharmacology
PG  - 98--103
VI  - 34
IP  - 2
4099  - http://molpharm.aspetjournals.org/content/34/2/98.short
4100  - http://molpharm.aspetjournals.org/content/34/2/98.full
SO  - Mol Pharmacol1988 Aug 01; 34
AB  - Single-channel currents were recorded by means of the patch clamp method in outside-out patches excised from rat cortical neurons in primary culture. The excitatory amino acid N-methyl-D-aspartic acid activated mainly 40-50 pS conductance channels. Channel opening durations were characterized by a series of rapid openings and closures induced by the presence of Mg2+ ions. This inhibitory effect was voltage dependent. Strychnine, the antagonist of the glycine-gated Cl- channels, blocks the N-methyl-D-aspartic acid-activated cationic channel in cultured rat cortical neurons. Strychnine action is voltage dependent and it is not counteracted by ethylenediaminetetraacetic acid, ruling out Mg2+ contamination of strychnine. It has been reported recently that glycine increases the rate of openings of N-methyl-D-aspartic acid-activated channels. This action is not affected by the presence of strychnine. Our results show that 1) Mg2+ and strychnine have an apparently similar intermediate blocking action on the NMDA-activated channels, 2) strychnine presumably acts as a sequential open channel blocker producing a different type of block compared with the one reported for Mg2+ ions, and 3) the lack of effect of strychnine on the glycine potentiation of the N-methyl-D-aspartic acid response indicates that this alkaloid does not competitively antagonize glycine but acts as an open channel blocker.