MEMBRANE-PROPERTIES OF RAT SUBICULAR NEURONS IN-VITRO

1. Conventional intracellular recordings were performed in rat hippoca mpal slices to investigate the electrophysiological properties of subi cular neurons. These cells had a resting membrane potential (RMP) of - 66 +/- 7.2 mV (mean +/- SD; n = 50), input resistance of 23.6 +/- 8.2 MOMEGA (n = 51), time constant of 7.1 +/- 1.9 ms (n = 51), action pote ntial amplitude of 85.8 +/- 13.8 mV (n = 50), and duration of 2.9 +/- 1.2 ms (n = 48). Analysis of the current-voltage relationship revealed membrane inward rectification in both depolarizing and hyperpolarizin g direction. The latter type was readily abolished by Cs+ (3 mM; n = 6 cells). 2. Injection of depolarizing current pulses of threshold inte nsity induced in all subicular neurons (n = 51) recorded at RMP a burs t of two to three fast action potentials (frequency = 212.7 +/- 90 Hz, n = 13 cells). This burst rode on a slow depolarizing envelope and wa s followed by an after hyperpolarization and later by regular spiking mode once the pulse was prolonged. Similar bursts were also generated upon termination of a hyperpolarizing current pulse. 3. The slow depol arization underlying the burst resembled a low-threshold response, whi ch in thalamic cells is caused by a Ca2+ conductance and is contribute d by the Cs+-sensitive inward rectifier. However, bursts in subicular cells persisted in medium containing the Ca2+-channel blockers Co2+ (2 mM) and Cd2+ ( 1 mM) (n = 5 cells) but disappeared during application of TTX (1 muM; n = 3 cells). Hence they were mediated by Na+. Blockad e of the hyperpolarizing inward rectification by Cs+ did not prevent t he rebound response (n = 3 cells). 4. Our findings demonstrate that in trinsic bursts, presumably related to a ''low-threshold'' Na+ conducta nce are present in rat subicular neurons. Similar intrinsic characteri stics have been suggested to underlie the rhythmic activity described in other neuronal networks, although in most cases the low-threshold e lectrogenesis was caused by Ca . We propose that the bursting mechanis m might play a role in modulating incoming signals from the classical hippocampal circuit within the limbic system.