TL;DR: In this paper, the number of GABA-expressing cells in neocortical slices is reduced by separating the neocortex from the subcortical telencephalon, and mice lacking the homeodomain proteins DLX-1/DLX-2 show no detectable cell migration from the cell to the brain.
Abstract: Although previous analyses indicate that neocortical neurons originate from the cortical proliferative zone, evidence suggests that a subpopulation of neocortical interneurons originates within the subcortical telencephalon. For example, gamma-aminobutyric acid (GABA)-expressing cells migrate in vitro from the subcortical telencephalon into the neocortex. The number of GABA-expressing cells in neocortical slices is reduced by separating the neocortex from the subcortical telencephalon. Finally, mice lacking the homeodomain proteins DLX-1 and DLX-2 show no detectable cell migration from the subcortical telencephalon to the neocortex and also have few GABA-expressing cells in the neocortex.
TL;DR: In conclusion, animal models demonstrate that the molecular basis of disruption is linked to specific defects in the development and function of interneurons — the cells that are responsible for establishing inhibitory circuits in the brain.
Abstract: The notion that the disruption of inhibitory circuits might underlie certain clinical features — notably cognitive impairment — in various neuropsychiatric disorders, including schizophrenia and autism, is receiving considerable attention. Focusing heavily on studies in animal models, Oscar Marin reviews the evidence indicating that the basis of such disruption is linked to specific defects in interneuron development and function.
TL;DR: Evidence that supports the existence of several tangential migration pathways in the telencephalon is reviewed, and recent findings that describe their regulation are summarized.
Abstract: Recent studies on the origin of cell populations in rodent and chicken embryonic brains provide evidence for extensive tangential migration within the developing telencephalon. On the basis of these findings, a new concept of corticogenesis has emerged, which proposes that two distinct neuronal populations cooperate in the formation of the cortex. One population consists of radially migrating neurons that originate in the ventricular zone of the pallium (cortex) and give rise to the glutamatergic pyramidal neurons. The second population consists of tangentially migrating neurons that originate in the ventricular zone of the subpallium (subcortical telencephalon) and give rise to GABA (γ-aminobutyric acid)-producing local circuit neurons. The subpallium is also the origin of other cell types that follow distinct tangential trajectories to migrate to structures such as the olfactory bulb and the striatum. Here, we review evidence that supports the existence of several tangential migration pathways in the telencephalon, and summarize recent findings that describe their regulation.
TL;DR: The cellular and molecular mechanisms underlying each of these types of migrations are reviewed and how emerging concepts in neuronal migration are reshaping the understanding of forebrain development in normal and pathological situations are discussed.
Abstract: The forebrain comprises an intricate set of structures that are required for some of the most complex and evolved functions of the mammalian brain. As a reflection of its complexity, cell migration in the forebrain is extremely elaborated, with widespread dispersion of cells across multiple functionally distinct areas. Two general modes of migration are distinguished in the forebrain: radial migration, which establishes the general cytoarchitectonical framework of the different forebrain subdivisions; and tangential migration, which increases the cellular complexity of forebrain circuits by allowing the dispersion of multiple neuronal types. Here, we review the cellular and molecular mechanisms underlying each of these types of migrations and discuss how emerging concepts in neuronal migration are reshaping our understanding of forebrain development in normal and pathological situations.
TL;DR: It is demonstrated that LGE and MGE cells migrate along different routes to populate distinct regions in the developing brain, and it is shown that the MGE is a major source of neurons migrating dorsally and invading the developing neocortex.
Abstract: Recent studies suggest that neurons born in the developing basal forebrain migrate long distances perpendicularly to radial glia and that many of these cells reach the developing neocortex. This form of tangential migration, however, has not been demonstrated in vivo, and the sites of origin, pathways of migration and final destinations of these neurons in the postnatal brain are not fully understood. Using ultrasound-guided transplantation in utero, we have mapped the migratory pathways and fates of cells born in the lateral and medial ganglionic eminences (LGE and MGE) in 13.5-day-old mouse embryos. We demonstrate that LGE and MGE cells migrate along different routes to populate distinct regions in the developing brain. We show that LGE cells migrate ventrally and anteriorly, and give rise to the projecting medium spiny neurons in the striatum, nucleus accumbens and olfactory tubercle, and to granule and periglomerular cells in the olfactory bulb. By contrast, we show that the MGE is a major source of neurons migrating dorsally and invading the developing neocortex. MGE cells migrate into the neocortex via the neocortical subventricular zone and differentiate into the transient subpial granule neurons in the marginal zone and into a stable population of GABA-, parvalbumin- or somatostatin-expressing interneurons throughout the cortical plate.