Figure 2. Pharmacological activation of acetylcholine receptors induces a variety of stable cellular and network oscillatory state.

Aa, intracellular recording from a CA3 pyramidal cell reveals a low frequency synchronous burst discharge in response to 1 μm carbachol application. Individual bursts (b) occur within a dominant frequency of 0.15 Hz, as shown in the power spectrum (c). Ba, higher concentration of carbachol (10 μm) results in the appearance of periodic episodes of rhythmic oscillatory depolarization. During oscillatory episodes, rhythmic depolarization was commonly suprathreshold resulting in a phasic dischage of action potentials (b) around the theta frequency range (c). Ca, in some slices, the predominant response to carbachol application is a persistent membrane potential oscillation within the high beta low–gamma frequency range, with the dominant frequency in this example (b) being 29 Hz. D, pharmacological uncoupling of fast AMPA receptor-mediated synaptic transmission (4 μm NBQX) reveals a very slow, presumably intrinsic oscillatory state in a subpopulation of pyramidal neurones, often resembling repeated plateau potentials. Oscillatory states described in A–C developed gradually as carbachol washed into the recording chamber. Each represents a sustained coherent activity within the hippocampal CA3 network that could be readily detected by extracellular field recordings. Oscillatory activity could also be induced rapidly as shown in E where arrowhead indicates fast application of 10 μm carbachol. Methodological details are given in Cobb et al. (1999) and Cobb et al. (2000).