Information processing and transfer between brain structures have been proposed to engage the phase-locking of neuronal firing to gamma oscillations during certain cognitive functions, including learning and memory. The cellular mechanism behind this precise temporal organisation of action potentials might rely on changes in synaptic strength. Kitanishi et al. (Kitanishi T, Ujita S, Fallahnezhad M, Kitanishi N, Ikegaya Y, Tashiro A. Neuron, 86:1265–76, 2015) tested this hypothesis by blocking synaptic plasticity dependent on the GluR1 subunit of AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptor using a virus-mediated local genetic manipulation in a restricted population of CA1 principal cells. Multi-tetrode-based unit recording from these genetically-modified principal cells showed that environmental novelty was associated with an impaired phase-locking to slow gamma oscillations and a slower emergence of precise spatial firing compared to control cells. This pattern of deficits suggests that CA3-driven slow gamma oscillations might induce GluR1-dependent synaptic plasticity in CA1. This cellular mechanism would in turn participate in the rapid emergence of precise place fields in CA1 during novel experiences, and in the transfer of this information to downstream neurons in a temporally-organised manner.