By Novartis Foundation
To appreciate the mind and its devastating illnesses, we have to exhibit the mechanisms that produce it and the ways that it may possibly continuously switch all through a lifetime. This booklet incorporates a well timed and insightful dialogue among developmental neurobiologists and clinicians who take care of problems of the worried procedure.
Chapters during this publication deal particularly with phone destiny decision, phone migration and issues of phone migration; present suggestions and new principles approximately cortical arealisation, and problems which may come up from improper arealisation; genes implicated within the improvement of cortical connectivity and similar pathologies reminiscent of schizophrenia and synaesthesia; and susceptibility genes for cognitive problems reminiscent of schizophrenia, autism, dyslexia, and a spotlight deficit disease.
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Extra info for Cortical Development: Genes and Genetic Abnormalities
A subset of the ones we originally published were areal specific only to those 5000–6000 corticospinal neurons. Neither Fez or Ctip2 define those populations alone; it is in combination with one or two other genes. Mallamaci: I have a question about Fez f2. Do we have any evidence that any discrepancy takes place between transcription of this gene and nuclear availability of the corresponding protein? In other words, is Fez f2 post-transcriptionally regulated? Is the protein regulated in its cytoplasmic or nuclear localization?
References Chen B, Schaevitz LR, McConnell SK 2005 Fez1 regulates the differentiation and axon targeting of layer 5 subcortical projection neurons in cerebral cortex. Proc Natl Acad Sci USA 102:17184–17189 Christophe E, Doerfl inger N, Lavery D, Molnár Z, Charpak S, Audinat E 2005 Two populations of layer V pyramidal cells of the mouse neocortex: Development and sensitivity to anesthetics. J Neurophysiol 94:3357–3367 Frantz GD, Bohner AP, Akers RM, McConnell SK 1994 Regulation of the POU domain gene SCIP during cerebral cortical development.
Goffinet: There is a large proportion of interneurons that are reelin positive. Where do they come from? Fishell: We haven’t looked at this. DEVELOPMENTAL ORIGINS OF CORTICAL INTERNEURON DIVERSITY 37 Goffinet: Has anyone looked at the origin of GABAergic interneurons in diencephalons. Could some of them come from the ganglionic eminence? Fishell: Michele Studer has some evidence arguing for this: that there is a migration back towards the diencephalons (Tripodi et al 2004). There are hints of that argument from the work from Pasko Rakic and Richard Sidman many years ago (Sidman & Rakic 1973).
Cortical Development: Genes and Genetic Abnormalities by Novartis Foundation