The GE may initiate migration because it expresses molecules that repulse interneurons. Semaphorins sema3a and sema3f in the lGE that affect interneurons through the neuropilins and plexin coreceptors. Chondrotin-4-sulfate work in coordination with semaphorins to propel interneurons through the lGE \cite{Kelsom_2013}. Slit1 also acts as a chemorepellent through the Roundabout (robo1) receptor on cortical interneurons \cite{Kelsom_2013}. Finally, ephrin and the ephrin receptor tyrosine kinases on interneurons also act as repulsive signal for MGE derived interneurons. CHECK SENTENCE ephrin 5a in the ventricular zone of the GE and receptor Epha4 is expressed by calbindin-expressing MGE-derived interneurons. \cite{Kelsom_2013}
Neuregulin 1 (Nrg1) is a protein (?) produced in the cortex that can guide mGE interneurons through the lGE and to the cerebral cortex. It has an epidermal growth-factor (EGF) domain that can activate the tyrosine kinase receptor ErB4 in interneurons \cite{Mar_n_2015}. Multiple types of Nrg1 can be expressed by the cortex and can have various effects \cite{Mar_n_2015} by modifying how interneurons extend neurites to produce their migration.
Another chemoattractant in the cortex is chenokine CXCL12 which changes over the course of embryonic development \cite{Kelsom_2013} . While it starts off high in the marginal zone and subventricular zone, it decreases in the subventricular zone. Interneurons from the mGE express CXCR4 and CXCR7 receptors \cite{Kelsom_2013} and are guided by CXCL12 to the cortex.
MGE derived interneurons colonize the cortex following the same inside0out sequence as pyramidal cells, so hat early born interneurons occupy ingragranular layers of the cortex, while late born interneurons primarily end up in supragranular layers.