1. Intracellular recordings were obtained from 184 distal apical dendrites and twenty-six somata of CA1 pyramidal neurones in the rat hippocampal slice preparation. In the presence of 3.25 mM K+ 200 ms suprathreshold current pulses evoked three different types of firing patterns in the apical dendrites, all of which were distinct from regular somatic firing. Past tetrodotoxin (TTX)-sensitive spiking was evoked in 38.8% of the dendrites. Compound spiking, consisting of an initial fast spike followed by one or more secondary slow spikes of variable amplitude and duration, was seen in 44.1% of dendrites. 'Classical' burst firing, resembling intrinsic somatic bursts, was evoked in 17.1% of the dendrites. 2. In fast spiking dendrites, the spikes evoked by long depolarizing pulses were rarely overshooting, showed prominent accommodation and declined progressively to about one-third of the initial amplitude. The amplitude of single dendritic fast spikes (50.6 +/- 1.5 mV; mean +/- S.E.M.) was smaller than that of somatic spikes (82.2 +/- 1.9 mV) and their rate of rise (81.3 +/- 4.3 V s(-1)) was markedly slower than that of somatic spikes (291.5 +/- 17.8 V s(-1)). However, the thresholds were not significantly different (dendrites, -49.8 +/- 0.8 mV; somata, -50.8 +/- 1.3 mV). These results indicate that fast spikes in the distal parts of apical dendrites are generated by a local regenerative Na+ current. 3. 4-Aminopyridine (4-AP, 0.1-0.5 mM) caused a dose-dependent slowing of the repolarization of the fast spikes, while tetraethylammonium (TEA, 2 mM) and Co2+ (2 mM) induced a slowing of the late phase of the repolarization. These results indicate that the transient outward K+ current, I-A, and the Ca2+-activated K+ current, I-C, are involved in the repolarization of dendritic Na+-dependent spikes. 4. Compound spiking was completely blocked by TTX (0.5-1 mu M). The secondary slow spikes within the complex were blocked by Co2+ (2 mM), nifedipine (10 mu M) and high concentrations (> 50 mu M) of verapamil, while Ni2+ (100-300 mu M) had no effect. Thus, compound spiking consists of an initial Na+-dependent spike followed by one or more slow Ca2+-dependent spikes mediated by L-type Ca2+ channels located in the apical dendrites. 5. In fast spiking dendrites, 4-AP (0.5-2.5 mM) changed the firing pattern from regular fast spiking to compound spiking. In the presence of 4-AP (0.1-0.5 mM), the single fast spike evoked by a short (20 ms), threshold current pulse, was followed by secondary slow spikes of variable amplitude and duration. This suggests that activation of a dendritic I-A has a significant influence on the spatial activation of dendritic L-type Ca2+ channels. 6. Increasing the extracellular K+ concentration to 5.25 mM had no effect on the passive membrane properties of the dendrites. However, the incidence of bursting dendrites increased to 83%, while the remaining 17% showed compound spiking. The burst responses were blocked by TTX (0.5-1 mu M), while Ni2+ (100-300 mu M), nifedipine (10 mu M) and verapamil (50-100 mu M) had no effect, indicating that neither T- nor L-type Ca2+ channels are involved in dendritic bursting.
