Based on a biophysical meanfield model, slow inhibitory interneuron population was introduced into the cortex to study absence seizures induced by cortical GABA receptors. it was found that inhibitory receptors GABAa and GABAb in pathway inhibitory interneuron population (IIN)excitatory pyramidal neuronal population (EPN) both participate in the control of absence seizures through introducing slow IIN. Especially, the appearance of spike and wave discharges (SWDs) is related to a scale factor K, which is defined as the relative strength of the receptors GABAa and GABAb. In addition, the slow kinetics of GABAb receptors is also a pathologic factor. Therefore, through the state analysis of scale factor K and the GABAB delay, it was found that they can jointly induce the absence seizures. These results provide a theoretical guidance on how the GABA receptors induce absence seizures, and may provide new insights into the treatment of this brain disease.