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Cerebello-cerebral connectivity in the developing brain.

ABSTRACT: Disrupted cerebellar development and injury is associated with impairments in both motor and non-motor domains. Methods to non-invasively characterize cerebellar afferent and efferent connections during early development are lacking. The aim of this study was to assess the feasibility of delineating cortico-ponto-cerebellar (CPC) and cerebello-thalamo-cortical (CTC) white matter tracts during brain development using high angular resolution diffusion imaging (HARDI). HARDI data were obtained in 24 infants born between 24⁺⁶ and 39 weeks gestational age (median 33⁺⁴ weeks) and scanned between 29⁺¹ and 44 weeks postmenstrual age (PMA) (median 37⁺¹ weeks). Probabilistic tractography of CPC and CTC fibers was performed using constrained spherical deconvolution. Connections between cerebellum and contralateral cerebral hemisphere were identified in all infants studied. Fractional anisotropy (FA) values of CTC and CPC pathways increased with increasing PMA at scan (p < 0.001). The supratentorial regions connecting to contralateral cerebellum in most subjects, irrespective of PMA at scan, included the precentral cortex, superior frontal cortex, supplementary motor area, insula, postcentral cortex, precuneus, and paracentral lobule. This study demonstrates the feasibility of assessing CTC and CPC white matter connectivity in vivo during the early stages of development. The ability to assess cerebellar connectivity during this critical developmental period may help improve our understanding of the role of the cerebellum in a wide range of neuromotor and neurocognitive disorders.

SUBMITTER: Pieterman K

PROVIDER: S-EPMC5406415 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature

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Cerebello-cerebral connectivity in the developing brain.

Pieterman Kay K Batalle Dafnis D Dudink Jeroen J Tournier J-Donald JD Hughes Emer J EJ Barnett Madeleine M Benders Manon J MJ Edwards A David AD Hoebeek Freek E FE Counsell Serena J SJ

Brain structure & function 20160829 4

Disrupted cerebellar development and injury is associated with impairments in both motor and non-motor domains. Methods to non-invasively characterize cerebellar afferent and efferent connections during early development are lacking. The aim of this study was to assess the feasibility of delineating cortico-ponto-cerebellar (CPC) and cerebello-thalamo-cortical (CTC) white matter tracts during brain development using high angular resolution diffusion imaging (HARDI). HARDI data were obtained in 2 ...[more]

PMID: 27573027

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Project description:Prenatal glucocorticoids prevent germinal matrix hemorrhage in premature infants. The underlying mechanism, however, is elusive. Germinal matrix is enriched with angiogenic vessels exhibiting paucity of pericytes and glial fibrillary acidic protein-positive astrocyte end feet. Therefore, we asked whether glucocorticoid treatment would suppress angiogenesis and enhance periendothelial coverage by pericytes and glial fibrillary acidic protein-positive end feet in the germinal matrix microvasculature.We treated pregnant rabbits with intramuscular betamethasone and delivered pups prematurely by cesarean section at E29 (term=32 days). Endothelial turnover, vascular density, pericyte coverage, glial fibrillary acidic protein-positive end feet, cell death, and growth factors orchestrating angiogenesis, including vascular endothelial growth factor, angiopoietins, transforming growth factor-beta, and platelet-derived growth factor-B, were compared between betamethasone-treated and untreated pups. Similar comparisons were done between autopsy materials from premature infants exposed and unexposed to prenatal glucocorticoids.Antenatal glucocorticoid treatment reduced endothelial proliferation, vascular density, and vascular endothelial growth factor expression in the germinal matrix of both rabbits and humans. The pericyte coverage was greater in glucocorticoid-treated rabbit pups and human infants than in controls, but not the glial fibrillary acidic protein-positive end feet coverage. Transforming growth factor-beta, but not angiopoietins and platelet-derived growth factor-B, were elevated in glucocorticoid-treated rabbit pups compared with controls. Betamethasone treatment induced apoptosis, neuronal degeneration, and gliosis in rabbit pups. However, there was no evidence of increased cell death in glucocorticoid-exposed human infants.Prenatal glucocorticoid suppresses vascular endothelial growth factor and elevates transforming growth factor-beta levels, which results in angiogenic inhibition, trimming of neovasculature, and enhanced pericyte coverage. These changes contribute to stabilizing the germinal matrix vasculature, thereby reducing its propensity to hemorrhage. Prenatal glucocorticoid exposure does not induce neural cell death in humans, unlike rabbits.

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Cerebello-cerebral connectivity in the developing brain.

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Cerebello-cerebral connectivity in the developing brain.

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