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. Author manuscript; available in PMC: 2009 Sep 22.
Published in final edited form as: Neuron. 2009 Jun 11;62(5):612–632. doi: 10.1016/j.neuron.2009.05.015

Figure 6.

Figure 6

Schematic representation of important experimental observations associated with ripple oscillations. A. Components that contribute to ripple oscillations. Consensus exists that the sharp wave produced by CA3 pyramidal neurons (blue) provides the excitatory drive that initiates the ripple oscillation. Also, it is generally accepted that rhythmic inhibition of CA1 pyramidal neurons (red) underlies ripple oscillations recorded in vivo. What is not clear is how such rhythmic inhibition arises (black box). One hypothesis suggests that rhythmogenic inhibitory networks provide input to CA1 pyramidal neurons (see Figure 7), while another argues that electrically coupled CA1 pyramidal neuron axons form the substrate for rhythmicity (see Figure 8). B. Graphical representation of observed activity patterns during ripple oscillation. Vertical lines placed on horizontal black lines represent extracellularly recorded action potentials of CA3 (blue) and CA1 (red) pyramidal neurons, and CA1 inhibitory neurons (green). The bottom red traces represent synaptic activity of an intracellularly recorded CA1 pyramidal neuron. Before the sharp wave all neurons are weakly active and synaptic activity observed in the CA1 pyramidal neuron is low (left panel). During the sharp wave CA3 pyramidal neurons fire highly synchronized bursts of action potentials, resulting in a moderate elevation of activity in CA1 pyramidal and inhibitory neurons. The sharp wave also causes a CA1 ripple oscillation, which is hypothesized to result from the fast rhythmic inhibition of CA1 pyramidal neurons.