Cell formation in the human hippocampal formation from mid-gestation to the late postnatal period

Seress, László; Ábrahám, Hajnalka; Tornóczky, Tamás; Kosztolányi, G.

doi:10.1016/s0306-4522(01)00156-7

Cited by 137 publications

(105 citation statements)

References 33 publications

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“…Except for the report on granule cells in the hippocampus (Eriksson et al, 1998), there are no signs of natural neuronal turnover in the human forebrain (Seress et al, 2001). However, it was reported recently that in the neocortex of adult rodents neurogenesis could be induced under a specific neurodegenerative con- dition, in particular after a photolytic deletion of projection neurons with the use of the retrograde transport of a dye and laser illumination (Magavi et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Nonrenewal of Neurons in the Cerebral Neocortex of Adult Macaque Monkeys

et al. 2003

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The concept that, after developmental periods, neocortical neurons become numerically stable and are normally nonrenewable has been challenged by a report of continuous neurogenesis in the association areas of the cerebral cortex in the adult Macaque monkey. Therefore, we have reexamined this issue in two different Macaque species using the thymidine analog bromodeoxyuridine (BrdU) as an indicator of DNA replication during cell division. We found several BrdUϩ/NeuNϩ (neuronal nuclei) double-labeled cells, but cortical neurons, distinguished readily by their size and cytological and immunohistochemical properties, were not BrdU positive. We examined in detail the frontal cortex, where it is claimed that the largest daily addition of neurons has been made, but did not see migratory streams or any sign of addition of new neurons. Thus, we concluded that, in the normal condition, cortical neurons of adult primates, similar to other mammalian species, are neither supplemented nor renewable.

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Section: Discussionmentioning

confidence: 99%

Nonrenewal of Neurons in the Cerebral Neocortex of Adult Macaque Monkeys

et al. 2003

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“…In rats and mice, embryonic days 11 to 18 (corresponding to day 56 of pregnancy through several months after birth in humans) is the critical period for development of the hippocampus and septum. 37 More choline (about 3 times the dietary levels) during days 11 to 18 of gestation results in increased cell proliferation and decreased apoptosis in rodent fetal hippocampal progenitor cells. 38,39 Morphological alterations occur in the brain after choline supplementation during fetal life, including larger soma and increased numbers of primary and secondary basal dendritic branches.…”

Section: Choline Availability Alters Brain Hippocampal Developmentmentioning

confidence: 99%

The fetal origins of memory: The role of dietary choline in optimal brain development

Zeisel

2006

The Journal of Pediatrics

194

140

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Fetal nutrition sets the stage for organ function in later life. In this review we discuss the fetal and neonatal origins of brain function. Numerous research observations point to the importance of choline for the developing fetus and neonate. This essential nutrient is involved in 1-carbon metabolism and is the precursor for many important compounds, including phospholipids, acetylcholine, and the methyl donor betaine. Dietary intake of choline by the pregnant mother and later by the infant directly affects brain development and results in permanent changes in brain function. In rodents, perinatal supplementation of choline enhances memory and learning functions, changes that endure across the lifespan. Conversely, choline deficiency during these sensitive periods results in memory and cognitive deficits that also persist. Furthermore, recent studies suggest that perinatal choline supplementation can reduce the behavioral effects of prenatal stress and the cognitive effects of prenatal alcohol exposure in offspring. The likely mechanism for these effects of choline involves DNA methylation, altered gene expression, and associated changes in stem cell proliferation and differentiation. The currently available animal data on choline and hippocampal development are compelling, but studies are needed to detrermine whether the same is true in humans.There is a growing body of evidence indicating that fetal and perinatal nutrition and growth influence organ function in adult life (eg, blood pressure, 1 heart disease, 2 diabetes 3 ). Evidence also indicates that fetal and perinatal nutrition influence brain function in later life. Iron, 4 zinc, 5 and folate 6 nutriture in the fetus have been shown to alter brain development, and there is compelling data showing that another important nutrient, choline, is essential for brain formation. The human requirement for choline was officially recognized with the establishment of adequate intake recommendations by the Institute of Medicine in 1998 7 (adequate intake for infants age 0 to 6 months, 18 mg/kg/day). Choline is required for the structural integrity and signaling functions of cell membranes, methyl group metabolism, and neurotransmitter synthesis. 8 Some of the choline needed to sustain normal organ function is synthesized de novo, mainly in the liver, 9 when phosphatidylethanolamine is methylated by phosphatidylethanolamine N-methyltransferase (PEMT) to form phosphatidylcholine. However, this mechanism does not always meet the demands for choline, and humans eating diets deficient in choline develop fatty liver, liver damage, and muscle damage. 10,11 In this review, the main focus is on choline's role in brain development and function during the perinatal period.

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“…For example, during the first postnatal weeks, neuronal birth, differentiation and migration are ongoing [4,53,16]. Neurogenesis of granule cells peaks during the second week of life in rodents [15] and during the third month in humans [129]. In addition, synaptogenesis and the establishment of enduring connectivity patterns continue for years in the human, and for weeks in the rodent [7].…”

Section: Enduring Effects Of Early-life Stress On Developing Hippocampusmentioning

confidence: 99%

Hippocampal neuroplasticity induced by early-life stress: Functional and molecular aspects

Fenoglio¹,

Brunson²,

Baram³

2006

Frontiers in Neuroendocrinology

189

138

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Whereas genetic factors contribute crucially to brain function, early-life events, including stress, exert long-lasting influence on neuronal function. Here, we focus on the hippocampus as the target of these early-life events because of its crucial role in learning and memory. Using a novel immaturerodent model, we describe the deleterious consequences of chronic early-life 'psychological' stress on hippocampus-dependent cognitive tasks. We review the cellular mechanisms involved and discuss the roles of stress-mediating molecules, including corticotropin releasing hormone, in the process by which stress impacts the structure and function of hippocampal neurons. KeywordsNeonatal; Rat; Human; Stress; Memory; Hippocampus; Corticotropin releasing hormone; CRF; Hypothalamic pituitary adrenal axis; Neuroplasticity Early-life events interact with genetic factors to influence hippocampal function long-termBrain function and dysfunction throughout life are determined by the interaction of genetic factors with 'acquired' environmental events, signals and stimuli [100]. Events that occur early in life are capable of exerting effects that persist throughout adulthood. Here, we focus on the hippocampus as the target of these early-life events because of its crucial role in learning, memory storage and retrieval, and general cognitive function [105,41,65]. Indeed, early-life events, via complex interactions with genetic factors [106,120], have been suspected to be a major determinant of smaller hippocampal volume and long-term cognitive dysfunction in preterm infants [111,17] and may play a role in certain affective and dementing disorders in the adult and aging human [100,26,120]. This review focuses on the mechanisms by which certain early-life events influence populations of hippocampal neurons acutely, and impact the function and integrity of the hippocampus long-term. Studying early-life stress may be used to probe the molecular mechanisms involved in experience-evoked hippocampal neuroplasticityStress may provide a salient example of early-life experience that might exert long-lasting influence on the brain, because (1) over 50% of the world's children are exposed to stress [139] and (2) evidence from both human and animal studies suggests that early-life stress has profound effects on cognitive function and emotional health.Stress has been shown to influence the hippocampus in a number of important ways. Whereas acute mild stress rapidly enhances synaptic efficacy and learning and memory processes [131,45,91,123], chronic or severe activation of the stress response early in life has been shown to be potentially injurious in both humans [6,120,147] and experimental animals [120,31]. For example, severe childhood psychological stress (neglect and abuse) correlates with a higher incidence of learning disabilities later in life, including those learning and memory functions requiring an intact hippocampus [121,50]. Further, MRI studies have suggested that adults subjected to abuse (a measure of chronic stress) ...

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Cell formation in the human hippocampal formation from mid-gestation to the late postnatal period

Cited by 137 publications

References 33 publications

Nonrenewal of Neurons in the Cerebral Neocortex of Adult Macaque Monkeys

Nonrenewal of Neurons in the Cerebral Neocortex of Adult Macaque Monkeys

The fetal origins of memory: The role of dietary choline in optimal brain development

Hippocampal neuroplasticity induced by early-life stress: Functional and molecular aspects

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