Astrocyte And Pathological States A Human Defects in Neuronal Migration

In the human, the major neuronal migrations that form the cortical plate occur by the 16th week of gestation, and late migrations from the germinal matrix into the cerebral cortex continue until 5 months postnatally. The external granule layer of the cerebel-lar cortex continues to migrate until 1 year of age.

Abnormalities of these migratory processes have pathological consequences.

The neural tube ofthe early human embryo is poorly vascularized. It may rely on the glial processes to transport nutrients between the ventricular system and the glycogen-rich meningeal tissue. Any pathological event, such as ischemia or hypoxia, that interrupts or distorts the radial glial fiber system between the ependymal and pial surfaces of the brain may create abnormalities of neuronal migration. If a premature infant suffers a subependymal hemorrhage, the radial glial process that is guiding neurons to the surface may retract from the cortical surface after its cell somata is destroyed. An immature neuron already in migration along this process may have escaped destruction within the zone of hemorrhage, but it is able to migrate only as far as the end of the glial guide fiber. The migrating cells in the company of several others whose radial fibers are also retracted for the same reason create a group of heterotopic cells that are unable to complete their journey. They mature in situ but are unable to establish their intended synaptic relations; consequently, there is a faulty synaptic circuitry. Failure of migrating cells to reach their proper destination may be referred to as neuronal ectopia. Incidental findings at autopsy may be related to the development of an epileptic focus.

In an animal model of Down's syndrome, the trisomy 16 mouse, there is a reduction of radial units in early telencephalic development, explaining the reduction in the final telencephalic size. Most mammals, including all primates, develop convolutions to provide a large cortical surface without incurring a concomitant increase in cerebral volume. Abnormal convolution patterns of the infant brain (i.e., pachy-gyria, lissencephaly, and polymicrogyria) are the result of faulty neuronal migration and are associated with an abnormally laminated cortex. Some of these are being characterized at the molecular level. The recently sequenced human gene for astrotactin, is a candidate for unsolved neuronal migration disorders in man. Even small perturbations can produce defects; abnormally migrated neurons and glia via a rupture of the glia limiting membrane have been found in the perisylvian cortex of some dyslexic brains.

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