CINs migrating from the MGE mature and ultimately form connections with excitatory pyramidal neurons in the neocortex. The identities and number of CINs relevant for signal processing differ depending on the spatial and temporal control of progenitor cells originating from the MGE. By maintaining the E/I balance, CINs are critical in promoting efficient information processing and higher cognitive functions 1, 2, 3. These results demonstrate that D-serine availability is essential for prenatal CIN development and postnatal cortical circuit maturation.Ĭortical interneurons (CINs) derived from the ventral medial ganglionic eminence (MGE) shape several aspects of cortical circuit maturation during development and maintain cortical excitatory-inhibitory (E/I) balance 1, 2, 3. In the PrL of postnatal day (PND) 16 SR −/− mice, there was a significant decrease in GAD67+ and PV+, but not SST + CIN density, which was associated with reduced inhibitory postsynaptic potentials in layer 2/3 pyramidal neurons. Lh圆 + cells develop into parvalbumin (PV+) and somatostatin (Sst+) CINs. At embryonic day 15, SR −/− mice had an accumulation of GABA and increased mitotic proliferation in the ganglionic eminence and fewer Gad1 + (glutamic acid decarboxylase 67 kDa GAD67) cells in the E18 neocortex. We found that most immature Lh圆 + CINs expressed SR and the obligatory NMDAR subunit NR1. We utilized constitutive SR knockout (SR −/−) mice to investigate the effect of d-serine availability on the development of CINs and inhibitory synapses in the prelimbic cortex (PrL). d-serine (co-agonist at many mature forebrain synapses) is racemized by the neuronal enzyme serine racemase (SR) from l-serine. NMDAR activation requires the binding of a co-agonist, either glycine or d-serine. Glutamate contributes to cortical interneuron (CIN) development via N-methyl- d-aspartate receptors (NMDARs). The proper development and function of telencephalic GABAergic interneurons is critical for maintaining the excitation and inhibition (E/I) balance in cortical circuits.
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