Abstract
This study investigates how NMDA and AMPA receptors influence synchronization in neural oscillators modeled by coupled Morris-Lecar systems. By analyzing the interplay between receptor kinetics, synaptic coupling strengths, and voltage-dependent magnesium block, we identify the mechanisms that govern neural synchronization. We show that fast AMPAR kinetics yield perfect synchrony at substantially lower coupling than NMDARs, which produce only near-synchrony even when Mg2+ block is absent. To resolve subtle regimes, we pair a time-domain mean phase difference (MPD) with the phase-locking value (PLV) and overlay bifurcation continuations (LP/HB/PD), exposing boundaries that PLV alone can miss. Although NMDARs sustain prolonged conductance, their slow decay and Mg2+ dependence blur spike timing and limit precise locking. These results provide a quantitative, mechanism-based account of glutamatergic control of synchrony and suggest experimentally testable predictions relevant to coordination deficits in disorders such as schizophrenia.