| 10601426 |
Tanabe M, Mori M, Gahwiler BH, Gerber U: Apamin-sensitive conductance mediates the K (+) current response during chemical ischemia in CA3 pyramidal cells. J Neurophysiol. 1999 Dec;82(6):2876-82.
Pyramidal cells typically respond to ischemia with initial transient hyperpolarization, which may represent a neuroprotective response. To identify the conductance underlying this hyperpolarization in CA3 pyramidal neurons of rat hippocampal organotypic slice cultures, recordings were obtained using the single-electrode voltage-clamp technique. Brief chemical ischemia (2 mM 2-deoxyglucose and 3 mM NaN (3), for 4 min) induced a response mediated by an increase in K (+) conductance. This current was blocked by intracellular application of the Ca (2+) chelator, bis-(o-aminophenoxy)-N,N,N', N'-tetraacetic acid (BAPTA), reduced with low external [Ca (2+)], and inhibited by a selective L-type Ca (2+) channel inhibitor, isradipine, consistent with the activation of a Ca (2+)-dependent K (+) conductance. Experiments with charybdotoxin (10 nM) and tetraethylammonium (TEA; 1 mM), or with the protein kinase C activator, phorbol 12,13-diacetate (PDAc; 3 microM), ruled out an involvement of a large conductance-type or an apamin-insensitive small conductance, respectively. In the presence of apamin (1 microM), however, the outward current was significantly reduced. These results demonstrate that in rat hippocampal CA3 pyramidal neurons an apamin-sensitive Ca (2+)-dependent K (+) conductance is activated in response to brief ischemia generating a pronounced outward current. |
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