Cortical interneuron development
The ganglionic eminences of the ventral telencephalon give rise to the striatum which emerges from the lateral ganglionic eminence (LGE), and to cortical and hippocampal GABA interneurons which are born in the medial and caudal ganglionic eminences (MGE and CGE). Parvalbumin (PV)+ and somatostatin (Sst)+ interneurons arise from the MGE, while calretinin+ interneurons arise largely from the CGE (Wonders et al., 2008). The interneurons from the MGE and CGE travel to the cortex via tangential migration during embryogenesis and progressively integrate into the cortical circuitry. Postnatally they undergo a protracted maturation and develop into their mature interneuron subtypes through processes that are largely unknown.
FGFR1 and FGFR2 appear to regulate early patterning of the ganglionic eminences before neurogenesis (Gutin et al., 2006). We shown that loss of fgfr1 or fgfr2 in the cerebral cortex via hgfap-Cre mediated recombination, which does not target the ganglionic eminences, results in a decrease in PV+ and Sst+ interneurons within the cortex (Smith et al., 2008). Work in our lab suggests that this deficit develops postnatally, and does not arise from defects in the patterning or proliferation of stem cells and progenitors in the ventral telencephalon. FGFR1 may act in the developing postnatal neocortex to support the survival and maturation of GABA interneurons.