A calcium-activated hyperpolarization follows repetitive firing in hippocampal neurons

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Abstract
A long-lasting afterhyperpolarization (AHP) follows current-induced repetitive firing in hippocampal CA1 neurons studied in vitro. A 10-25% increase in membrane slope conductance occurs during the AHP, suggesting that it may be mediated by an increased conductance to either K+ or Cl-. Intracellular Cl- iontophoresis does not alter the AHP but does attenuate the IPSP [inhibitory post-synaptic potential]. Ba2+, a cation that can decrease K+ conductance, eliminates the AHP but not the IPSP. The AHP is perhaps produced by a long-lasting increased conductance to K+, and is distinct from the IPSP. Mn2+, a Ca2+-channel blocker, eliminates the AHP. The AHP persists in the presence of the Na+-channel blocker, tetrodotoxin (TTX) and appears to be temporally associated with TTX-resistant Ca2+ spikes. AHP is probably activated by CA2+ influx. The AHP may be produced by a Ca2+ activated K+ current. A balance between cellular depolarization produced by Ca2+ entry and repolarization generated by a Ca2+-activated K+ current appears to operate to control excitability in some mammalian cortical neurons as it does in molluscan neurons. Disruption of this balance by Ba2+ produces spontaneous membrane-potential oscillations and recurrent burst firing in hippocampal neurons. Increases in the magnitude and duration of Ca2+ depolarization and/or decreases in the Ca2+-activated, K+-mediated repolarization may be mechanisms that lead to spontaneous, epileptiform bursting in mammalian cortical neurons.