The ganglionic eminence (GE) is a transitory structure in the development of the nervous system that guides cell and axon migration.

[1] It is present in the embryonic and fetal stages of neural development found between the thalamus and caudate nucleus.

The cells of the GEs are quite homogenous, with the MGE, LGE, and CGE all having small, dark, irregular nuclei and moderately dense cytoplasm, however, each eminence can be identified by the type of progeny that it produces.

Additionally, the subventricular zone is the starting point of multiple streams of tangentially migrating interneurons that express Dlx genes.

[2] The primary purpose of the MGE during development is to produce GABAergic stellate cells and direct their migration to the neocortex.

Compared to the early temporal frame of development in the MGE, the LGE aids in the tangential migration of cells later in the mid-embryogenic stage.

The route that newly generated neurons take from the anterior subventricular zone to the olfactory bulb is called the rostral migratory stream.

[6] The CGE is a fusion of the rostral medial and lateral ganglionic eminence, which begins at the mid to caudal thalamus.

[3] Cells in the LGE migrate to the striatal domain (caudate nucleus and putamen) and parts of the septum and amygdala.

The function of the molecules that affect migration are not confined to cell movement, overlapping considerably with the events associated with neurogenesis.

Zellweger Syndrome is characterized by a cortical dysplasia similar to polymicrogyria of cerebral and cerebellar cortex, occasionally with pachygyria surrounding the Sylvian fissure, and focal/subependymal heterotopia.

Kallmann syndrome is recognized by anosmia associated with mental retardation, hypogonadism, and the failure of the olfactory bulb to develop.

Disorders of axonal projection and assembly are rarely pure, but closely related to neuronal migration genes.

Examples include ectopic neurogenesis, microencephaly, and altered cell survival resulting in areas of hyperplasia, reduced apoptosis, and heterotopia.

The complexity of molecular steps needed to correctly place cells in a system as complicated as the brain is impressive, and as more pieces to this intricate puzzle arise, it will be easier to come up with strategies to remedy disorders associated with neuronal migration, and to potentially repair damage caused by trauma, stroke, maldevelopment, and aging.