Rescuing astroglial VMAT2 and DA levels in the critical postnatal period during which spines are subject to DA regulation [12, 30] corrects the cognitive abnormalities in VMAT2-deficient mice, and therefore suggests that defective synaptic structures and functions developed in the third postnatal week may crucially contribute to dysregulating PFC neural networks and promote the genesis of cognitive deficits. The gene discussed is SLC18A2; the disease is Cognitive impairment.