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Strychnine‐induced potassium current in CA1 pyramidal neurones of the rat hippocampus
Author(s) -
Ebihara Satoru,
Akaike Norio
Publication year - 1992
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1992.tb14419.x
Subject(s) - chemistry , biophysics , strychnine , tetraethylammonium , tetraethylammonium chloride , membrane potential , patch clamp , 4 aminopyridine , reversal potential , glibenclamide , electrophysiology , potassium channel , channel blocker , bapta , intracellular , endocrinology , potassium , medicine , biochemistry , biology , receptor , calcium , organic chemistry , diabetes mellitus
1 Direct actions of strychnine (Str) and brucine (Bru) on the dissociated hippocampal CA1 neurones of the rat have been investigated with the whole‐cell mode of the patch‐clamp technique. 2 At a holding potential (V H ) of − 20 mV, both Str and Bru elicited outward current at concentrations over 10 −5 m . The reversal potential of Str‐induced current (E Str ) was − 77.8 mV, which was close to the K + equilibrium potential (E K = − 80.3 mV). The change in E Str for a ten fold change in extracellular K + concentration was 58 mV, indicating that the membrane behaves like a K + electrode in the presence of Str. 3 The concentration‐response curves for Str and Bru were bell‐shaped, and nearly maximum response occurred at 10 −4 m for Str and 3 × 10 −4 m for Bru. The maximum current amplitude induced by Bru was about 80% of that induced by Str. A transient ‘hump’ current appeared immediately after the wash‐out of external solutions containing Str and Bru at concentrations higher than 10 −4 and 3 × 10 −4 m , respectively. 4 The Str‐induced current ( I Str ) was antagonized by K + channel blockers such as Ba 2+ , tetraethylammonium (TEA)‐chloride, and 4‐aminopyridine (4‐AP) in a concentration‐dependent manner. I Str was insensitive to glibenclamide, a blocker of ATP‐sensitive K + channels. 5 Internal perfusion with 10 m m BAPTA did not affect the Str‐induced I K . Depletion of the intracellular Ca 2+ store by caffeine had no effect, indicating that intracellular Ca 2+ does not mediate the Str‐induced activation of K + conductance. 6 Both guanosine‐5′‐O‐3‐thiotriphosphate (GTPγS) and guanosine‐5′‐O‐thiodiphosphate (GDPβS) suppressed the Str‐induced I K , the former action appearing more rapidly than the latter. The results suggest that the GTP binding proteins are involved in this Str response. 7 When neurones were loaded with cholera toxin (CTX) or pertussis toxin (PTX) through a patch pipette, PTX suppressed the Str response whereas CTX did not, suggesting that G i and/or G o might be involved in the Str‐induced I K .