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Voltage‐clamp analysis of the potentiation of the slow Ca 2+ ‐activated K + current in hippocampal pyramidal neurons
Author(s) -
Borde Michel,
Bonansco Christian,
Fernández de Sevilla David,
Le Ray Didier,
Buño Washington
Publication year - 2000
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/(sici)1098-1063(2000)10:2<198::aid-hipo9>3.0.co;2-f
Subject(s) - long term potentiation , chemistry , neuroscience , hippocampal formation , intracellular , biophysics , depolarization , patch clamp , electrophysiology , biology , biochemistry , receptor
Exploring the principles that govern activity‐dependent changes in excitability is an essential step to understand the function of the nervous system, because they act as a general postsynaptic control mechanism that modulates the flow of synaptic signals. We show an activity‐dependent potentiation of the slow Ca 2+ ‐activated K + current (sI AHP ) which induces sustained decreases in the excitability in CA1 pyramidal neurons. We analyzed the sI AHP using the slice technique and voltage‐clamp recordings with sharp or patch‐electrodes. Using sharp electrodes‐repeated activation with depolarizing pulses evoked a prolonged (8‐min) potentiation of the amplitude (171%) and duration (208%) of the sI AHP . Using patch electrodes, early after entering the whole‐cell configuration (<20 min), responses were as those reported above. However, although the sI AHP remained unchanged, its potentiation was markedly reduced in later recordings, suggesting that the underlying mechanisms were rapidly eliminated by intracellular dialysis. Inhibition of L‐type Ca 2+ current by nifedipine (20 μM) markedly reduced the sI AHP (79%) and its potentiation (55%). Ryanodine (20 μM) that blocks the release of intracellular Ca 2+ also reduced sI AHP (29%) and its potentiation (25%). The potentiation of the sI AHP induced a marked and prolonged (>50%; ≈8 min) decrease in excitability. The results suggest that sI AHP is potentiated as a result of an increased intracellular Ca 2+ concentration ([Ca 2+ ] i ) following activation of voltage‐gated L‐type Ca 2+ channels, aided by the subsequent release of Ca 2+ from intracellular stores. Another possibility is that repeated activation increases the Ca 2+ ‐binding capacity of the channels mediating the sI AHP . This potentiation of the sI AHP could be relevant in hippocampal physiology, because the changes in excitability it causes may regulate the induction threshold of the long‐term potentiation of synaptic efficacy. Moreover, the potentiation would act as a protective mechanism by reducing excitability and preventing the accumulation of intracellular Ca 2+ to toxic levels when intense synaptic activation occurs. Hippocampus 10:198–206, 2000 © 2000 Wiley‐Liss, Inc.