Gamma oscillations (30-70 Hz) have been hypothesized to play a role in cortical function. Most of the proposed mechanisms involve rhythmic modulation of neuronal excitability at gamma frequencies, leading to modulation of spike timing relative to the rhythm. I first show that the gamma band could be more privileged than other frequencies in observing spike-field interactions even in the absence of genuine gamma rhythmicity and discuss several biases in spike-gamma phase estimation. I then discuss the expected spike-gamma phase according to several hypotheses. Inconsistent with the phase-coding hypothesis (but not with others), the spike-gamma phase does not change with changes in stimulus intensity or attentional state, with spikes preferentially occurring 2-4 ms before the trough, but with substantial variability. However, this phase relationship is expected even when gamma is a byproduct of excitatory-inhibitory interactions. Given that gamma occurs in short bursts, I argue that the debate over the role of gamma is a matter of semantics.
Keywords: LFP; gamma; local field potential; oscillations; phase; visual cortex.