Recordings of epileptiform burst activity in the CA1 region of the transverse rat hippocampal slices were made with a 32-channel surface electrode array. The 200 μm interelectrode resolution, the simultaneity of the data, and the use of a two-dimensional current source density analysis allowed accurate measurement of population spike peak times. Differences were found in the apparent propagation delays among 3 burst components: the compound action potential (CAP) along the Schaffer collaterals, the first population spike directly driven by the CAP, and the second (and succeeding) population spikes representing the bursting, epileptiform component. Delay measurements were applied to epileptiform bursts recorded in slices treated with picrotoxin (PTX), pentylenetetrazol (PTZ), and 0-Mg 2+ medium. In 0-Mg 2+ medium all components propagate at nearly the same velocity. In the PTZ and PTX media the second population spike propagated more slowly than the CAP. The first population spike propagated at the same velocity as the CAP for orthodromic Schaffer collateral stimulation. The first population spike propagated at the same, slower velocity as the second spike for antidromic Schaffer collateral stimulation.