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Principles of neuromotor development
Published in Mijna Hadders-Algra, Kirsten R. Heineman, The Infant Motor Profile, 2021
Mijna Hadders-Algra, Kirsten R. Heineman
The development of the cerebellum has its own timing. Cells in the cerebellum originate from two proliferative zones: (1) the ventricular zone which brings forth the deep cerebellar nuclei and the Purkinje cells, and (2) the external granular layer originating from the rhombic lip (Volpe 2009b). Cell proliferation in the cerebellum starts at 11 weeks PMA in the ventricular zone and at 15 weeks in the external granular layer. The external granular layer is a transient structure reaching its peak thickness between 28 and 34 weeks PMA. It produces the most numerous cells of the cerebellum, the granule cells. These cells migrate from the external granular layer inward to their final destination in the internal granular layer. The latter grows most prominently between mid-gestation and three months post-term. The external granular layer shrinks, in particular between two and three months post-term. However, it takes until the second half of the first postnatal year for the external granular layer to dissolve entirely (Hadders-Algra 2018a).
Developmental Diseases of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
James H. Tonsgard, Nikolas Mata-Machado
Formation of the mature nervous system is dependent on the induction or formation of precursor cells, followed by the proliferation and maturation of cells within periventricular germinal centers and finally, migration to their intended sites. A cross section of the developing brain shows that it is initially organized into an outer pial (preplate) or marginal zone (MZ) and inner ventricular zone (VZ) (Figure 9.4a). Stem cells proliferate and differentiate into immature neurons and glial precursors within the VZ and subventricular zone (SVZ). Starting in the seventh fetal week, neuroblasts in the VZ migrate upward to form a subpial preplate zone (PP). Subsequently, neurons migrate into the PP (Figure 9.4c1). These neurons divide, with some forming the superficial molecular layer or MZ (layer I) and others moving to the deep subplate. Thereafter, waves of neurons pass through the subplate, successively forming layers VI, V, IV, III, and II in an inside-out pattern, with the last neurons moving into layer II (Figure 9.4b, c3).
VIP Regulation of Neuronal Proliferation and Differentiation
Published in Sami I. Said, Proinflammatory and Antiinflammatory Peptides, 2020
The nervous system regulates diverse body functions, from the relatively “simple” and automatic (vegetative), such as respiration, to the highly integrative and complex, such as cognition and memory. The neurons of the peripheral (PNS) and central nervous system (CNS) underlying these functional differences are produced from proliferating precursors or neuroblasts (8). Significantly, precursors of different neuronal populations exhibit distinct and highly characteristic patterns of neuro-genesis: Precursors proliferate for varying periods of time, at different locations, and with lineage-specific relationships of mitosis to differentiation. For example, rat cerebral cortex precursors proliferate for 2—4 days in the densely aggregated neural tube ventricular zone. Following cessation of proliferation, neurons migrate to their final cortical position as they undergo differentiation (8). In contrast, peripheral sympathetic neuroblasts arise from the migratory neural crest cells that proliferate for 11 days at their final tissue destination, expressing multiple differentiated traits while actively dividing (8—11). Finally, cerebellar granule neurons, involved in motor coordination, are generated during the first three postnatal weeks, in a displaced ventricular zone overlying the cerebellum, and neurons migrate only after elaborating axonal processes (8).
Continuum modeling for neuronal lamination during cerebral morphogenesis considering cell migration and tissue growth
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2021
Hironori Takeda, Yoshitaka Kameo, Taiji Adachi
Cerebral tissue has a well-ordered layered structure consisting of several subtypes of neurons, the formation of which plays an essential role in acquiring physiological brain functions (Rakic 2009). To understand cerebral morphogenesis, it is important to clarify the mechanisms governing the formation of the neuronal layers. Neuronal lamination is accomplished through neuronal migration and accumulation during cerebral morphogenesis. Neurons are produced from radial glial progenitor cells in the ventricular zone (VZ) (Borrell and Reillo 2012; Borrell and Gotz 2014), which is located in the inner region of the cerebrum. The neurons then migrate along the radial glial cells toward the marginal zone (MZ) (Rakic 1972; Borrell and Reillo 2012; Borrell and Gotz 2014), which is located close to the cerebral surface. After reaching the MZ, the neurons stop their migration and accumulate to form an inside-out layered structure in a cortical plate (CP), where the late-born neurons are arranged outside of the early-born neurons (Marin et al. 2010).
Are Nestin-positive cells responsive to stress?
Published in Stress, 2020
Stefan R. Bornstein, Ilona Berger, Charlotte Steenblock
Neurons are generated from early embryonic development until early postnatal stages, with only a few neurogenic zones remaining active in the adult (Paridaen & Huttner, 2014). In the adult human brain, neurogenesis is restricted to two main niches: the sub-ventricular zone (SVZ) of the lateral ventricles and the sub-granular zone (SGZ) of the dentate gyrus (DG) in the hippocampus. Neural stem cells (NSCs) residing in the SVZ dgenerate neurons that migrate to the olfactory bulb, while in the hippocampal SGZ, radial glia-like NSCs give rise to new dentate granule neurons. These hippocampal neurons contribute to memory and cognitive functions, as well as to the processing of emotions and the regulation of stress responses (Cameron & Schoenfeld, 2018; Dranovsky & Leonardo, 2012). In addition to their neural fate, in order to constrain and/or prevent tissue damage, NSCs from both SVZ and SGZ may turn into both astroglial and oligodendroglial cells, which means a rather gliogenic than neurogenic response (Butti et al., 2014).
Congenital Visual Field Loss from a Schizencephalic Cleft Damaging Meyer’s Loop
Published in Neuro-Ophthalmology, 2021
Benyam Kinde, A. James Barkovich, Jonathan C. Horton
Patients with Col4A1 mutations have been reported whose neuroimaging shows a schizencephalic cleft that closely resembles the lesion in our patient (for example, see Figure 2l in Yoneda et al.7). However, our patient, like most patients with a schizencephalic cleft, had no identifiable genetic mutation.12,14 This means that other genetic mutations causing prenatal vascular rupture remain to be discovered or that the event in our patient was a sporadic vascular accident. Alternatively, the lesion might have resulted from failure of stem cells in a segment of the ventricular zone to generate the radial columns of cells required to form the cortical plate.