Rostral migratory stream

In the adult subgranular zone (SGZ), dense clusters of dividing cells were found to be anatomically close to the vasculature, especially capillaries.

[7] Astrocytes form gap junctions[8] and are closely associated with the vasculature and its basal lamina in the adult SVZ and subsequently in the RMS.

In addition, astrocytes derived from the neurogenic hippocampus and SVZ, but not from the non-neurogenic spinal cord, promote proliferation and neuronal fate commitment of multipotent adult neural stem cells in culture, suggesting a role in the RMS.

Astrocytes express a number of secreted and membrane-attached factors both in vitro and in vivo that are known to regulate proliferation and fate specification of adult neural precursors as well as neuronal migration, maturation, and synapse formation.

Under basal conditions, apoptotic corpses of newly generated neurons are rapidly phagocytosed from the niche by unactivated microglia in the adult SGZ.

Under inflammatory conditions, reactivated microglia can have both beneficial and detrimental effects on different aspects of adult neurogenesis, depending on the balance between secreted molecules with pro- and anti-inflammatory action.

[12] Developing neurons leave the subventricular zone and enter the RMS and travel caudally and ventrally along the undersurface of the caudate nucleus; this is referred to as the descending limb.

Once the developing neurons reach the core of the olfactory bulb, they detach from the RMS, which is initiated by Reelin and tenascin[16] and move radially toward glomeruli, this migration is dependent on tenascin-R,[16] and differentiate into subtypes of interneurons.

It has been demonstrated that a cross talk exists between neurons and glial cells and data in favor of an active role of PSA–NCAM in this process has been presented.

The lack of PSA–NCAM on the surface of migrating precursors might alter the proliferative properties of this glial cell population, a scenario that appears reminiscent of astrogliosis occurring in neurodegenerative diseases even before any signs of neuronal damage.

In the developing fetal brain and in young postnatal infants, chains of immature neurons typical of the RMS were observed.

They discovered that cells that expressed DCX (doublecortin) and PSA-NCAM are present in the brain sections taken from infants, but have disappeared by 18 months.

However, a direct correlation between stem cell quiescence and age has not yet been defined due to a high level of variability between individuals.

[22] Furthermore, age-related declines in the activities of SVZ stem cells, which migrate to the OB via the RMS, are in place by middle age in rodents.

In elderly mice, studies showed that the population of actively dividing SVZ cells and the rate of interneuron replacement in the OB are both drastically reduced, indicating an age-related decline in neuronal proliferation and migration through the RMS.

This decline was shown to be due to neuronal stem cell quiescence in the SVZ even by middle age, and not destruction, much like in the hippocampus.

[24] In this study, the experimenters disrupted the RMS in mice, which obstructed “the uptake of intranasally administered radioligands into the CNS.” Fluorescent tracers were also used to track the medicine throughout the brain.

The study concluded that the RMS was extremely prevalent and necessary in the central nervous system in order to deliver drugs intranasally.