In the suprachiasmatic nucleus (SCN), γ-aminobutyric acid (GABA) is a primary neurotransmitter. GABA can signal through two types of GABAAreceptor subunits, often referred to as synaptic GABAA(gamma subunit) and extra-synaptic GABAA(delta subunit). To test the functional roles of these distinct GABAAin regulating circadian rhythms, we developed a multicellular SCN model where we could separately compare the effects of manipulating GABA neurotransmitter or receptor dynamics. Our model predicted that blocking GABA signalling modestly increased synchrony among circadian cells, consistent with published SCN pharmacology. Conversely, the model predicted that lowering GABAAreceptor density reduced firing rate, circadian cell fraction, amplitude and synchrony among individual neurons. When we tested these predictions, we found that the knockdown of delta GABAAreduced the amplitude and synchrony of clock gene expression among cells in SCN explants. The model further predicted that increasing gamma GABAAdensities could enhance synchrony, as opposed to increasing delta GABAAdensities. Overall, our model reveals how blocking GABAAreceptors can modestly increase synchrony, while increasing the relative density of gamma over delta subunits can dramatically increase synchrony. We hypothesize that increased gamma GABAAdensity in the winter could underlie the tighter phase relationships among SCN cells.