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Novel action of BAPTA series chelators on intrinsic K + currents in rat hippocampal neurones
Author(s) -
Lancaster B.,
Batchelor A. M.
Publication year - 2000
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2000.t01-1-00231.x
Subject(s) - bapta , chemistry , biophysics , conductance , current (fluid) , intracellular , biochemistry , physics , biology , condensed matter physics , thermodynamics
1 Whole‐cell recordings were made from rat CA1 neurones in brain slices. When electrodes contained diazo‐2 (2 m m ) or dibromo BAPTA (1 m m ) a large steady‐state outward current (hundreds of picoamps) developed within 5 min of breakthrough at a V H of −60 mV. BAPTA itself (1 m m ) caused qualitatively similar but smaller effects. 2 The outward current was accompanied by increased conductance with a null potential close to the calculated K + equilibrium potential ( E K ) of −110 mV. Development of outward current occurred concurrently with progressive loss of slow AHP tail current ( I sAHP ) evoked by brief depolarizations. The peak latency of I sAHP increased during the onset of chelator action. 3 The persistent outward current was reversibly inhibited by noradrenaline (10 μ m ) or isoprenaline (2–5 μ m ), and completely prevented by 8‐bromoadenosine 3′,5′ cyclic monophosphate (8‐Br cAMP; 100 μ m ) or QX‐314 (10 m m ) in recording electrodes. After development of outward current, diazo‐2 photolysis caused inward current and decreased conductance. Both flash‐ and noradrenergic‐sensitive responses were inwardly rectifying outward currents with null potentials close to E K . 4 The outward current induced by dibromo BAPTA was not blocked by internal EGTA (10 m m ). However, experiments incorporating Ca 2+ influx or Ca 2+ loading of the buffer indicate that Ca 2+ facilitated the outward current. 5 The outward currents induced by dibromo BAPTA or diazo‐2 were not associated with significant changes in resting [Ca 2+ ] i . Regions of the cell contributing to the outward current were deduced from measurements of fura‐2 diffusion. These were compared with regions of [Ca 2+ ] i elevation during I sAHP . 6 These results are consistent with the hypothesis that the BAPTA series Ca 2+ buffers can activate those Ca 2+ ‐activated K + channels that underlie the slow AHP, without the predicted elevation of bulk [Ca 2+ ] i . Therefore these results cannot be interpreted solely in terms of Ca 2+ concentration changes, although the observations illustrate a novel, investigative role for these compounds in the study of Ca 2+ ‐dependent processes.