Figure 2.

Rhythmic CA1 pyramidal neurons and theta (θ): in vitro and in vivo recordings. (A1) Representative in vitro patch recordings showing θ–like membrane potential oscillations and action potential bursts induced by NMDA microiontophoresis at the apical dendrites of a CA1 pyramidal neuron (upper); superfision of AP5 blocked the NMDA response (lower). (A2) As (A1), but another neuron showing the effects of NMDA microiontophoresis in control ringer. (A3) Superfusion of TTX abolished action potential bursting but oscillations, NMDA- and Ca²⁺-spikes remained. (B1) Representative in vivo recordings of spontaneous CA1 EEG (upper) and CA1 neuron showing typical θ oscillations and single and occasional action potential bursts (lower). (B2,3) Same as (B1) in a CA3 neuron showing slow spikes riding on a sustained depolarization and firing rhythmic action potential bursts time-locked with θ oscillations; the red dots in (A3) correspond to the superimposed expanded records in panel (C). (D1) Representative in vivo tonic discharge evoked by a depolarizing current pulse applied immediately after impalement with a QX314-filled electrode. (D2) Record obtained later after impalement showing a slow putative Ca²⁺ spike and fewer and smaller action potentials. (D3,4) Even later, action potentials were blocked and one and two slow spikes were triggered with increasing pulse intensities (1–4 same neuron). (A) Modified from Bonansco and Buño (2003); (B,C) modified from Núñez et al. (1987); (D) modified from Nuñez and Buño (1992).