1. 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-. 2. Intracellular Cl- iontophoresis does not alter the AHP but does attenuate the IPSP. In contrast Ba2+, a cation that can decrease K+ conductance, eliminates the AHP but not the IPSP. These findings suggest the AHP is produced by a long-lasting increased conductance to K+, and is distinct from the IPSP. 3. Mn2+, a Ca2+-channel blocker, eliminates the AHP. In comparison, the AHP persists in the presence of the Na+-channel blocker, tetrodotoxin (TTX), and appears to be temporally associated with TTX-resistant "Ca2+ spikes." It is concluded that AHP is probably activated by Ca2+ influx. 4. These observations indicate that 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.

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1. Anomalous rectification occurred in 54 of 56 hippocampal CA1 neurons studied in vitro. This phenomenon is characterized by a progressive increase in input resistance with membrane depolarization. An average increase in membrane resistance of 45% occurred over a 15-mV region of membrane potential immediately subthreshold to cellular firing. 2. Both Mn2+, a Ca+ antagonist, and tetrodotoxin (TTX), a neurotoxin that blocks regenerative Na+ currents, eliminated anomalous rectification. Ba2+, which can both contribute to intracellular cation influx as well as reduce K+ conductance, increased the magnitude of anomalous rectification. The observations are indirect evidence indicating that a Ca2+-Na+ current may produce the inward-going rectification. 3. Enhancement of anomalous rectification by Ba2+ was associated with the onset of membrane oscillations and spontaneous bursts of repetitive discharges. The magnitude of anomalous rectification may be one factor that predisposes some cortical neurons to bursting behavior.