Afterpotential generation in hippocampal pyramidal cells.

Abstract

Intracellular recordings were obtained from CA3 pyramidal cells in guinea pig hippocampal slices maintained in vitro. As in the case of CA1 pyramidal neurons, CA3 cells show nonlinear current-voltage relations (I-V) and an apparent decrease in input resistance on hyperpolarization in the subthreshold range (anomalous rectification). The input resistance was 38 .+-. 12.7 M.OMEGA. (mean .+-. SD) in 15 neurons. The membrane time constant was 30.5 .+-. 6.2 ms. Spontaneous spike-firing patterns were influenced by the resting membrane potential, and prominent burst firing tended to occur when the membrane potential was in the range between -65 and -55 mV. At more depolarized levels solitary spiking became the predominant activity. CA3 pyramidal neurons generated high-threshold tetrodotoxin-resistant, presumed Ca spikes during depolarization. Depolarizing afterpotentials (DAP), which followed single directly evoked orthdromic or antidromic spikes, had both active and passive components. The active component could be blocked by Mn2+ and facilitated by Ba2+, suggesting that it was mediated by a Ca2+ conductance, activated by the Na+ spike. The passive phase of the DAP was resistant to Mn2+ and its time course paralleled that of the passive charging of the membrane. This passive component was a consequence of termination of spike repolarization at a slightly depolarized level. Following single spikes, burst of spikes or presumed Ca2+ spikes, prolonged afterhyperpolarizations (AHP) occurred. The characteristics of the AHP, including the associated conductance increase and sensitivity to Mn2+, were similar to those reported in CA1 neurons for AHP mediated by a Ca2+-activated K+ conductance. Intrinsically generated DAP and AHP provide a mechanism for generation and patterning of spontaneous and evoked burst firing. Highly stereotyped bursts can be generated in the absence of patterned synaptic input. These bursts are similar to those recorded in CA3 pyrimidal neurons following exposure to the convulsant agent penicillin.