scholarly journals Placental, Matrilineal, and Epigenetic Mechanisms Promoting Environmentally Adaptive Development of the Mammalian Brain

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Kevin D. Broad ◽  
Eridan Rocha-Ferreira ◽  
Mariya Hristova
Keyword(s):  
Genomic Imprinting ◽  
Neural Plasticity ◽  
Information Transfer ◽  
Developing Brain ◽  
Mammalian Brain ◽  
Neural Function ◽  
Mammalian Development ◽  
Intrauterine Development ◽  
Epigenetic Information ◽  
Ultimate Control

The evolution of intrauterine development, vivipary, and placentation in eutherian mammals has introduced new possibilities and constraints in the regulation of neural plasticity and development which promote neural function that is adaptive to the environment that a developing brain is likely to encounter in the future. A range of evolutionary adaptations associated with placentation transfers disproportionate control of this process to the matriline, a period unique in mammalian development in that there are three matrilineal genomes interacting in the same organism at the same time (maternal, foetal, and postmeiotic oocytes). The interactions between the maternal and developing foetal hypothalamus and placenta can provide a template by which a mother can transmit potentially adaptive information concerning potential future environmental conditions to the developing brain. In conjunction with genomic imprinting, it also provides a template to integrate epigenetic information from both maternal and paternal lineages. Placentation also hands ultimate control of genomic imprinting and intergenerational epigenetic information transfer to the matriline as epigenetic markers undergo erasure and reprogramming in the developing oocyte. These developments, in conjunction with an expanded neocortex, provide a unique evolutionary template by which matrilineal transfer of maternal care, resources, and culture can be used to promote brain development and infant survival.

scholarly journals DNA modifications in the mammalian brain

2014 ◽  
Vol 369 (1652) ◽  
pp. 20130512 ◽  
Author(s):  
Jaehoon Shin ◽  
Guo-li Ming ◽  
Hongjun Song
Keyword(s):  
Dna Methylation ◽  
Brain Development ◽  
Genomic Imprinting ◽  
Mammalian Brain ◽  
Epigenetic Mark ◽  
Mammalian Development ◽  
Dna Modifications ◽  
Dna Elements ◽  
And Function ◽  
Neuronal Functions

DNA methylation is a crucial epigenetic mark in mammalian development, genomic imprinting, X-inactivation, chromosomal stability and suppressing parasitic DNA elements. DNA methylation in neurons has also been suggested to play important roles for mammalian neuronal functions, and learning and memory. In this review, we first summarize recent discoveries and fundamental principles of DNA modifications in the general epigenetics field. We then describe the profiles of different DNA modifications in the mammalian brain genome. Finally, we discuss roles of DNA modifications in mammalian brain development and function.

Neuroplasticity

2019 ◽  
pp. 230-260
Author(s):  
Judy S. Reilly ◽  
Lara R. Polse
Keyword(s):  
Neural Plasticity ◽  
Late Onset ◽  
Neural Substrates ◽  
Brain Regions ◽  
Developing Brain ◽  
Perinatal Stroke ◽  
Alternative Pathways ◽  
Affective Expression ◽  
Unilateral Brain ◽  
Irreparable Damage

With respect to language, it has long been observed that children who experience early unilateral brain injury do not show the same irreparable damage as do adults with homologous late-onset strokes. Neural plasticity has been proposed as the explanation for such differential linguistic profiles; that is, the plasticity of the young, developing brain allows the possibility for extensive adaptation and organization following a neural insult. Recent research, however, suggests that there are limits to this ability to adapt and organize. Results from a another communicative system, affect, suggest that children with unilateral pre- or perinatal stroke show similar (albeit subtler) effects to adults with homologous late-onset injuries. This chapter presents findings on language development in children who sustained a pre- or perinatal unilateral stroke, and complements these studies with a discussion of affective expression in these same children. These prospective studies of children with perinatal stroke provide a unique window into the development of the neural substrates for language and affect. Specifically, they afford a context to investigate the degree to which particular brain regions may be privileged for specific behavioral functions, as well as how the developing brain adapts to organize alternative pathways in the wake of an early insult.

scholarly journals The Expression and Distributions of ANP32A in the Developing Brain

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Shanshan Wang ◽  
Yunliang Wang ◽  
Qingshan Lu ◽  
Xinshan Liu ◽  
Fuyu Wang ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Fetal Brain ◽  
Tissue Expression ◽  
Developing Brain ◽  
Adult Brain ◽  
Mammalian Brain ◽  
Dependent Manner ◽  
Growing Up ◽  
Embryonic Mouse ◽  
And Function

Acidic (leucine-rich) nuclear phosphoprotein 32 family, member A (ANP32A), has multiple functions involved in neuritogenesis, transcriptional regulation, and apoptosis. However, whether ANP32A has an effect on the mammalian developing brain is still in question. In this study, it was shown that brain was the organ that expressed the most abundant ANP32A by human multiple tissue expression (MTE) array. The distribution of ANP32A in the different adult brain areas was diverse dramatically, with high expression in cerebellum, temporal lobe, and cerebral cortex and with low expression in pons, medulla oblongata, and spinal cord. The expression of ANP32A was higher in the adult brain than in the fetal brain of not only humans but also mice in a time-dependent manner. ANP32A signals were dispersed accordantly in embryonic mouse brain. However, ANP32A was abundant in the granular layer of the cerebellum and the cerebral cortex when the mice were growing up, as well as in the Purkinje cells of the cerebellum. The variation of expression levels and distribution of ANP32A in the developing brain would imply that ANP32A may play an important role in mammalian brain development, especially in the differentiation and function of neurons in the cerebellum and the cerebral cortex.

Applying Basic Neuroscience to Aphasia Therapy

1995 ◽  
Vol 4 (4) ◽  
pp. 88-93 ◽  
Author(s):  
Kristen A. Keefe
Keyword(s):  
Learning And Memory ◽  
Neural Plasticity ◽  
Behavioral Interventions ◽  
Cortical Reorganization ◽  
Mammalian Brain ◽  
Cortical Injury ◽  
Aphasia Therapy ◽  
Neural Processes ◽  
Adult Mammalian Brain ◽  
Environmental Demands

Advances in basic neuroscience have increased our knowledge about the neural processes underlying learning and memory and the cortical reorganization that occurs in response to environmental demands and cortical injury. This article provides a selective review of published studies conducted in animals that examine functional and structural substrates of neural plasticity in the adult mammalian brain, and discusses the implications of this knowledge for aphasia therapy. The processes and constraints identified in the studies reviewed can be used to refine and justify current aphasia therapies, as well as to design additional behavioral interventions.

scholarly journals Glycans and glycosaminoglycans in neurobiology: key regulators of neuronal cell function and fate

2018 ◽  
Vol 475 (15) ◽  
pp. 2511-2545 ◽  
Author(s):  
Anthony J. Hayes ◽  
James Melrose
Keyword(s):  
Cell Fate ◽  
Information Transfer ◽  
Cell Function ◽  
Dermatan Sulfate ◽  
Neuronal Cell ◽  
Keratan Sulfate ◽  
Neural Function ◽  
Cellular Survival ◽  
Downstream Signaling ◽  
Blood Group Substances

The aim of the present study was to examine the roles of l-fucose and the glycosaminoglycans (GAGs) keratan sulfate (KS) and chondroitin sulfate/dermatan sulfate (CS/DS) with selected functional molecules in neural tissues. Cell surface glycans and GAGs have evolved over millions of years to become cellular mediators which regulate fundamental aspects of cellular survival. The glycocalyx, which surrounds all cells, actuates responses to growth factors, cytokines and morphogens at the cellular boundary, silencing or activating downstream signaling pathways and gene expression. In this review, we have focused on interactions mediated by l-fucose, KS and CS/DS in the central and peripheral nervous systems. Fucose makes critical contributions in the area of molecular recognition and information transfer in the blood group substances, cytotoxic immunoglobulins, cell fate-mediated Notch-1 interactions, regulation of selectin-mediated neutrophil extravasation in innate immunity and CD-34-mediated new blood vessel development, and the targeting of neuroprogenitor cells to damaged neural tissue. Fucosylated glycoproteins regulate delivery of synaptic neurotransmitters and neural function. Neural KS proteoglycans (PGs) were examined in terms of cellular regulation and their interactive properties with neuroregulatory molecules. The paradoxical properties of CS/DS isomers decorating matrix and transmembrane PGs and the positive and negative regulatory cues they provide to neurons are also discussed.

Maintenance of complex neural function during perfusion of the mammalian brain

1987 ◽  
Vol 409 (1) ◽  
pp. 128-132 ◽  
Author(s):  
George B. Richerson ◽  
Peter A. Getting
Keyword(s):  
Mammalian Brain ◽  
Neural Function

scholarly journals Multiple Imprinted Genes Associated with Prader-Willi Syndrome and Location of an Imprinting Control Element

1996 ◽  
Vol 45 (1-2) ◽  
pp. 87-89
Author(s):  
R.D. Nicholls ◽  
M.T.C. Jong ◽  
C.C. Glenn ◽  
J. Gabriel ◽  
P.K. Rogan ◽  
...  
Keyword(s):  
Genomic Imprinting ◽  
Epigenetic Modification ◽  
Uniparental Disomy ◽  
Paternal Allele ◽  
Control Element ◽  
Parental Origin ◽  
Imprinted Genes ◽  
Mammalian Development ◽  
Specific Expression ◽  
Large Deletions

Our studies aim to identify the mechanisms and genes involved in genomic imprinting in mammalian development and human disease. Imprinting refers to an epigenetic modification of DNA that results in parent-of-origin specific expression during embryogenesis and in the adult. This imprint is reset at each generation, depending on the sex of the parental gametogenesis. Prader-Willi (PWS) and Angelman (AS) syndromes are excellent models for the study of genomic imprinting in humans, since these distinct neurobehavioural disorders are both associated with genetic abnormalities (large deletions, uniparental disomy, and imprinting mutations) of inheritance in chromosome 15q11-q13, dependent on the parental origin (reviewed in ref. 1). Some AS patients have biparental inheritance, consistent with a single imprinted gene (active on the maternal chromosome), whereas similar PWS patients are not found suggesting that at least two imprinted genes (active on the paternal allele) may be necessary for classical PWS. We have previously shown that the small ribonucleoprotein associated protein SmN gene (SNRPN), located in the PWS critical region [2], is only expressed from the paternal allele and is differentially methylated on parental alleles [3]. Therefore, SNRPN may have a role in PWS. Methylation imprints have also been found at two other loci in 15q11-q13, PW71 [4] and D15S9 [5], which map 120 kb and 1.5 Mb proximal to SNRPN, respectively. We have now characterized in detail the gene structure and expression from two imprinted loci within 15q11-q13, SNRPN and D15S9, which suggests that both loci are surprisingly complex, with important implications for the pathogenesis of PWS.

scholarly journals Parental prey selection affects risk-taking behaviour and spatial learning in avian offspring

2007 ◽  
Vol 274 (1625) ◽  
pp. 2563-2569 ◽  
Author(s):  
Kathryn E Arnold ◽  
Scot L Ramsay ◽  
Christine Donaldson ◽  
Aileen Adam
Keyword(s):  
Spatial Learning ◽  
Risk Taking ◽  
Prey Selection ◽  
Learning Task ◽  
Control Treatment ◽  
Mammalian Brain ◽  
Mammalian Development ◽  
Cyanistes Caeruleus ◽  
Novel Objects ◽  
Spatial Learning Task

Early nutrition shapes life history. Parents should, therefore, provide a diet that will optimize the nutrient intake of their offspring. In a number of passerines, there is an often observed, but unexplained, peak in spider provisioning during chick development. We show that the proportion of spiders in the diet of nestling blue tits, Cyanistes caeruleus , varies significantly with the age of chicks but is unrelated to the timing of breeding or spider availability. Moreover, this parental prey selection supplies nestlings with high levels of taurine particularly at younger ages. This amino acid is known to be both vital and limiting for mammalian development and consequently found in high concentrations in placenta and milk. Based on the known roles of taurine in mammalian brain development and function, we then asked whether by supplying taurine-rich spiders, avian parents influence the stress responsiveness and cognitive function of their offspring. To test this, we provided wild blue tit nestlings with either a taurine supplement or control treatment once daily from the ages of 2–14 days. Then pairs of size- and sex-matched siblings were brought into captivity for behavioural testing. We found that juveniles that had received additional taurine as neonates took significantly greater risks when investigating novel objects than controls. Taurine birds were also more successful at a spatial learning task than controls. Additionally, those individuals that succeeded at a spatial learning task had shown intermediate levels of risk taking. Non-learners were generally very risk-averse controls. Early diet therefore has downstream impacts on behavioural characteristics that could affect fitness via foraging and competitive performance. Fine-scale prey selection is a mechanism by which parents can manipulate the behavioural phenotype of offspring.

Genomic imprinting and mammalian development

Placenta ◽  
1996 ◽  
Vol 17 (1) ◽  
pp. 3-14 ◽  
Author(s):  
G FRANKLIN ◽  
G ADAM ◽  
R OHLSSON
Keyword(s):  
Genomic Imprinting ◽  
Mammalian Development
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