Observations of heterogeneity among the principal cell populations of the neocortex and the subiculum have been described previously in the literature (Behr et al. 1996; Pineda et al. 1999). Heterogeneity among hippocampal principal cells has been suspected for some time, but has not been conclusively proven. Here we describe two populations of CA1 pyramidal cell distinguished on the basis of their afterpotential profiles.

Intracellular recordings of CA1 pyramidal cells were made from 450 µm hippocampal slices, obtained from male adult Wistar rats weighing approximately 150 g. Animals were killed humanely after being anaesthetised with inhaled isoflurane, before intramuscular injection with xylazine (> 10 mg kg^-1) and ketamine ( > 100 mg kg^-1). Rats were cardioperfused with sucrose ACSF. Data are expressed as mean amplitude ± standard error of the mean.

Recordings revealed that pyramidal cells expressed one of two types of slow AHP after short (80 ms duration) depolarising current steps. Type I sAHP was preceded by a medium afterhyperpolarisation (mAHP) and was almost completely inhibited by application of 20 µM 5-HT (control = 4.97 ± 1.3 mV, 5HT = 0.80 ± 0.3 mV, n = 6, P = 0.016, paired t test). Cells that expressed type I sAHP usually fired single spikes during depolarising steps, although not exclusively. Type II sAHP had a shorter duration than type I and was not preceded by a mAHP. Cells expressing this form of sAHP generally fired bursts of action potentials. Type II sAHP was significantly attenuated by 5HT application (control = 8.8 ± 2.0 mV, 5HT = 4.8 ± 1.9 mV, n = 5, P = 0.04 paired t test). The ratio of hyperpolarisation amplitude to number of action potentials per burst was greater for type II sAHP than type I sAHP. The two forms of sAHP showed varying sensitivity to nifedipine. Type I sAHP was largely insensitive to 20 µM nifedipine (control = 3.2 ± 0.31 mV, nifedipine = 3.19 ± 0.55 mV, n = 5, P = 0.9 paired t test), whereas type II sAHP was significantly reduced by nifedipine (control = 8.2 ± 0.78 mV, nifedipine = 4.1 ± 1.3 mV, n = 3, P = 0.002 paired t test).

We suggest that calcium entry through L-type calcium channels is required to activate type II sAHP, but not essential to activate type I sAHP. These results suggest that there is heterogeneity among the principal cell population of the CA1 area of the hippocampus.

This work was generously funded by the MRC UK and GSK plc.