Membrane properties of rat subicular neurons in vitro

D. Mattia, G. G C Hwa, M. Avoli

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Abstract

1. Conventional intracellular recordings were performed in rat hippocampal slices to investigate the electrophysiological properties of subicular 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 MΩ (n = 51), time constant of 7.1 ± 1.9 ms (n = 51), action potential 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 hyperpolarizing direction. The latter type was readily abolished by Cs+ (3 mM; n = 6 cells). 2. Injection of depolarizing current pulses of threshold intensity induced in all subicular neurons (n = 51) recorded at RMP a burst of two to three fast action potentials (frequency = 212.7 ± 90 Hz, n = 13 cells). This burst rode on a slow depolarizing envelope and was 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 depolarization underlying the burst resembled a low-threshold response, which in thalamic cells is caused by a Ca2+ conductance and is contributed 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 μM; n = 3 cells). Hence they were mediated by Na+. Blockade of the hyperpolarizing inward rectification by Cs+ did not prevent the rebound response (n = 3 cells). 4. Our findings demonstrate that intrinsic bursts, presumably related to a 'low-threshold' Na+ conductance are present in rat subicular neurons. Similar intrinsic characteristics have been suggested to underlie the rhythmic activity described in other neuronal networks, although in most cases the low-threshold electrogenesis was caused by Ca2+. We propose that the bursting mechanism might play a role in modulating incoming signals from the classical hippocampal circuit within the limbic system.

Original languageEnglish
Pages (from-to)1244-1248
Number of pages5
JournalJournal of Neurophysiology
Volume70
Issue number3
Publication statusPublished - 1993

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ASJC Scopus subject areas

  • Physiology
  • Neuroscience(all)

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