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J Neurophysiol 78: 1256-1262, 1997;
0022-3077/97 $5.00
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The Journal of Neurophysiology Vol. 78 No. 3 September 1997, pp. 1256-1262
Copyright ©1997 The American Physiological Society

Properties of a Ca2+-Activated K+ Conductance in Acutely Isolated Pyramidal-Like Neurons From the Rat Basolateral Amygdaloid Complex

S. Meis and H.-C. Pape

Institut für Physiologie, Otto-von-Guericke-Universität, D-39120 Magdeburg, Germany

Meis, S. and H.-C. Pape. Properties of a Ca2+-activated K+ conductance in acutely isolated pyramidal-like neurons from the rat basolateral amygdaloid complex. J. Neurophysiol. 78: 1256-1262, 1997. A calcium (Ca2+)-activated potassium (K+) conductance was studied in large pyramidal-like neurons acutely dissociated from the rat basolateral amygdaloid complex. Neurons were immunoreactive to anti-alpha (913-926), a sequence-directed antibody directed against the pore-forming alpha -subunit of the BKCa channel, also termed slo. Whole cell current-voltage (I-V) relationships obtained on application of slow (46.7 mV/s) voltage ramps from -110 to +100 mV were N shaped positive to -30 mV. Maximal current activation occurred at +9.8 ± 2.7 (SE) mV, with a mean current density of 404.8 ± 25.0 pA/pF. Substitution of extracellular Ca2+ with manganese (Mn2+), or with magnesium (Mg2+) and addition of 5 mM ethyleneglycol-bis(beta -aminoethylether)-N,N,N',N'-tetraacetic acid, abolished the N-shaped I-V relationship with a reduction in maximal outward current to 15.3 ± 2.3% of the control value. The Ca2+-sensitive K+ current component, as revealed by voltage step protocols, activated at depolarizations positive to -30 mV with a slow time course (time constant 430.7 ± 78.6 ms). The current was reduced by 80.4 ± 4.6% through 1 mM tetraethyammonium chloride and by 66.8 ± 3.4% through 100 nM iberiotoxin, whereas apamin up to 1 µM had no effect. It is concluded that pyramidal-like neurons of the basolateral amygdaloid complex possess BKCa channels and the corresponding macroscopic Ca2+-sensitive K+ conductance, activation of which will substantially contribute to the Ca2+-dependent regulation of electrogenic behavior in these neurons.




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