INTRODUCTION: Synchronized neural oscillations enable coherent communication across distributed cortical networks and depend on precisely regulated excitation–inhibition feedback circuits. AMPA-type glutamate receptors (AMPARs) mediate rapid excitatory transmission and are therefore central to temporally precise network coordination. However, their causal role in shaping large-scale oscillatory synchronization in primates remains insufficiently understood.

AIM(S): We investigated whether acute AMPAR blockade modulates spontaneous and stimulus evoked neural oscillations in a non-human primate model.

METHOD(S): Electroencephalography (EEG) was recorded during resting-state (not task or stimulus related) and 40-Hz auditory steady-state responses (ASSRs) in the common marmoset (Callithrix jacchus, n=6) before and after administration of the selective, non-competitive AMPAR antagonist perampanel, with saline as a control. Spectral power density and phase synchronization measures were applied to quantify network-level oscillatory dynamics.

RESULTS: Preliminary results show that AMPAR antagonism increased low-frequency power during resting state and reduced phase-locked 40-Hz responses during auditory stimulation. Early event-related potentials were decreased in amplitude and temporally delayed, suggesting disrupted temporal integration of fast excitatory inputs within cortical circuits.

CONCLUSIONS: These findings demonstrate that AMPAR-mediated fast excitatory transmission contributes to both spontaneous and entrained oscillatory synchronization. By linking synaptic AMPAR function to broadband EEG dynamics, this study advances mechanistic understanding of how glutamatergic signaling shapes coordinated neural activity across temporal scales.

FINANCIAL SUPPORT: Hakubi Center Grant