A major challenge in the field of neuroscience is to understand how the brain transitions from an immature state to a mature state. Early brain development is a period of heightened plasticity, during which sensory experience helps the brain mature. This plasticity is lost with progressing age; however, loss of plasticity is disadvantageous to patients with traumatic brain injury or certain neurodevelopmental disorders because loss of brain plasticity is not readily repairable. Neuroscience research has linked a neurotransmitter called γ-amino butyric acid (GABA) with this gradual loss of brain plasticity. Understanding how GABAergic signaling regulates brain maturation is important for advancing treatments for traumatic brain injury and neurological disorders. Using the hamster visual system, we have shown that contrary to common belief, early life light exposure is not necessary for visual system development, but rather for maintenance of the developed visual system in adulthood. Hamsters raised in darkness from birth exhibited normal visual development initially but were unable to maintain that development past puberty. This correlated with decreased GABA and decreased synaptic GABAA receptor (GABAAR) efficacy in dark-reared (DR) animals. However, the specific role played by the postsynaptic GABAergic signaling components in visual deprivation-related reduction in adult visual refinement remains unidentified. In this thesis work, we exclude several possible mechanisms that could explain the reduced activation of GABAARs previously reported in the superior colliculus (SC) and visual cortex (VC) of dark reared adult hamsters, supporting the idea that activity-dependent regulation of GABA expression is the primary mechanism underlying maintenance of RF refinement. The finding that a change in GABA levels alone could affect visual refinement in adulthood has important implications for the treatment of memory impairments or brain injury.