Searching for ways out of the autism maze: genetic, epigenetic and environmental clues

The reelin gene encodes an extracellular protein that is crucial for neuronal migration in laminated brain regions. To gain insights into the functions of Reelin, we performed high-resolution in situ hybridization analyses to determine the pattern of reelin expression in the developing forebrain of the mouse. We also performed double-labeling studies with several markers, including calcium-binding proteins, GAD65/67, and neuropeptides, to characterize the neuronal subsets that express reelin transcripts. reelin expression was detected at embryonic day 10 and later in the forebrain, with a distribution that is consistent with the prosomeric model of forebrain regionalization. In the diencephalon, expression was restricted to transverse and longitudinal domains that delineated boundaries between neuromeres. During embryogenesis, reelin was detected in the cerebral cortex in Cajal-Retzius cells but not in the GABAergic neurons of layer I. At prenatal stages, reelin was also expressed in the olfactory bulb, and striatum and in restricted nuclei in the ventral telencephalon, hypothalamus, thalamus, and pretectum. At postnatal stages, reelin transcripts gradually disappeared from Cajal-Retzius cells, at the same time as they appeared in subsets of GABAergic neurons distributed throughout neocortical and hippocampal layers. In other telencephalic and diencephalic regions, reelin expression decreased steadily during the postnatal period. In the adult, there was prominent expression in the olfactory bulb and cerebral cortex, where it was restricted to subsets of GABAergic interneurons that co-expressed calbindin, calretinin, neuropeptide Y, and somatostatin. This complex pattern of cellular and regional expression is consistent with Reelin having multiple roles in brain development and adult brain function.

https://www.jneurosci.org/content/jneuro/18/19/7779.full.pdf

Regional and cellular patterns of reelin mRNA expression in the forebrain of the developing and adult mouse

An astonishing number of extracellular matrix glycoproteins are expressed in dynamic patterns in the developing and adult nervous system. Neural stem cells, neurons, and glia express receptors that mediate interactions with specific extracellular matrix molecules. Functional studies in vitro and genetic studies in mice have provided evidence that the extracellular matrix affects virtually all aspects of nervous system development and function. Here we will summarize recent findings that have shed light on the specific functions of defined extracellular matrix molecules on such diverse processes as neural stem cell differentiation, neuronal migration, the formation of axonal tracts, and the maturation and function of synapses in the peripheral and central nervous system.

/pdf/extracellular-matrix-functions-in-the-nervous-system-520idp1kha.pdf

Extracellular Matrix: Functions in the Nervous System

Cellular and genetic regulation of the development of the cerebellar system.

The development of the mammalian cerebellum is orchestrated by both cell-autonomous programs and inductive environmental influences. Here, we describe the main processes of cerebellar ontogenesis, highlighting the neurogenic strategies used by developing progenitors, the genetic programs involved in cell fate specification, the progressive changes of structural organization, and some of the better-known abnormalities associated with developmental disorders of the cerebellum.

/pdf/consensus-paper-cerebellar-development-if424wuguo.pdf

Consensus Paper: Cerebellar Development.

The development of the cerebellum has been studied in normal and reeler mice, from embryonic day fourteen, i.e. when morphogenesis begins in this organ, to birth. The cerebellar nuclei develop according to a similar sequence in both genotypes. Their neurons migrate into the rostral field of the cerebellar bud where they condense in a rounded mass, well defined at E14. From E17, this cell contingent spreads transversally and the three roof nuclei become clearly defined. In reeler mutants, there seems to be an abnormal development of the architectonics of the lateral nucleus. The Purkinie cells migrate into the cortex at the same time in both genotypes. In the normal animal,from E14 onward, Purkinje cells are condensed in a clearly defined plate, where they assume a radial organization. By contrast, the mutant Purkinje cells are not arranged in a plate but are scattered in the periphery of the cortex. The neurons of the external granular layer are identical in both genotypes. Radial glial fibers and early Golgi epithelial cells appear to be normally present in the reeler embryo. The foliation of the cerebellar cortex begins at E17 in the normal embryo. From this stage onward, foliation is increasingly deficient in reeler mutants. Based on these observations, it is suggested that, in normal cerebellar development, a specific, genetically determined mechanism is responsible for the organization and the stabilization of postmigratory neurons and that this mechanism is affected by the reeler mutation.

The embryonic development of the cerebellum in normal and reeler mutant mice

The cerebral cortex of reeler (rl/rl) and control (rl/+) embryos has been examined at embryonic day 14 (E0=day of the plug). At this early stage, the cells of the cortical plate in reeler are characteristically maloriented when compared to the controls but, despite this malorientation, they assume a normal differentiation; in particular the regions of contact between the cells of the cortical plate are not different from the controls. The marginal zone and the subcortical plate of reeler are less well delimited than in normal fetuses, yet each of these layers contains the same contingent of cells and fibers as the normal embryos. In particular an early afferent fiber system is visualized in reeler and shows the same characteristics as in normal embryos: weak osmiophily, presence of dense core vesicles and of multilocular dense vacuoles, formation of asymmetric synapses in the marginal zone. The nature of these fibers is unknown but it is suggested that they could correspond to the aminergic system described in rats at the same developmental stage. The observations reported, though compatible with the hypothesis that the reeler gene acts upon a cell recognition-adhesion phenomenon between CP cells, do not provide a positive evidence for it and do not exclude other explanations.

The Cerebral-cortex of the Reeler Mouse Embryo - An Electron-microscopic Analysis

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The embryonic development of the cerebellum in normal and reeler mutant mice

The Cerebral-cortex of the Reeler Mouse Embryo - An Electron-microscopic Analysis