Absence seizures are classified as genetic generalized seizures. They arise from abnormalities in corticothalamic networks evident as spike-wave discharges on electroencephalograms. Altered gamma-aminobutyric acid (GABA) neurotransmission is commonly reported in rodent models for absence seizures. However, the underlying causative mechanism for seizures at the cellular and molecular level is debated and appears multifactorial, which may account for the variable efficacy of antiepileptic drugs. Current drugs fail to suppress seizures in over 30% of children with absence epilepsy. Previously, we demonstrated that dysfunctional feed-forward-inhibition (FFI) is implicated as one cause of absence seizures. In the stargazer mouse model of absence epilepsy loss of FFI is accompanied by changes in gamma-aminobutyric acid receptor (GABAR) expression; phasic GABAAR subunits are decreased in the somatosensory cortex but increased in the ventroposterior thalamus. The current study aimed to identify the developmental time-course for region-specific changes in corticothalamic GABAergic networks to determine if they directly contribute to absence seizures generation. Biochemical fractionation and semiquantitative Western blot analyses were used to investigate levels of GABAAR subunit expression in synaptic and cytosolic fractions of somatosensory cortex and thalamic lysates at critical developmental stages before and after seizure onset. We found no significant changes in synaptic GABAAR in postnatal mice immediately before seizure onset. Therefore changes in phasic GABARs are unlikely to directly contribute to the initiation of absence seizures but rather are a consequence of seizure activity. GABAAR plasticity could be an attempt to balance hyperexcitability. However, such changes could also contribute to further pathogenesis of absence epilepsy.