Afterpotential generation in hippocampal pyramidal cells

Intracellular recordings were obtained from CA3 pyramidal cells in 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 MΩ (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- (TTX) resistant, presumed calcium spikes during depolarization. Depolarizing afterpotentials (DAPs), 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 sodium 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 after-hyperpolarizations (AHPs) occurred. The characteristics of the AHP, including the associated conductance increased and sensitivity to Mn²⁺, were similar to those reported in CA1 neurons for AHPs mediated by a CA²⁺-activated K⁺ conductance. Intrinsically generated DAPs and AHPs provide a mechanism for generation and patterning of spontaneous and evoked burst firing. Highly stereotyped bursts can thus be generated in the absence of patterned synaptic input. These bursts appear to be similar to those recorded in CA3 pyrimidal neurons following exposure to the convulsant agent penicillin.