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495 results for “brain development”
Impacts of development and adult sex on brain cell numbers in the Black Soldier Fly, Hermetia illucens L. (Diptera: Stratiomyidae)
<p>The Black Soldier Fly (<em>Hermetia illucens</em>, Diptera: Stratiomyidae) has been introduced across the globe, with numerous industry applications predicated on its tremendous growth during the larval stage. However, basic research on <em>H. illucens</em> biology (for example, studies of their central nervous system) are lacking. Despite their small brain volumes, insects are capable of complex behaviors; understanding how these behaviors are completed with such a small amount of neural tissue requires understanding processing power (e.g. number of cells) within the brain. Brain cell counts have been completed in only a few insect species (mostly Hymenoptera), and almost exclusively in adults. This limits the taxonomic breadth of comparative analyses, as well as any conclusions about how development and body size growth may impact brain cell populations. Here, we present the first images and cell counts of the <em>H. illucens</em> brain at four time points across development (early, mid, and late larval stages, and both male and female adults) using immunohistochemistry and isotropic fractionation. To assess sexual dimorphism in adults, we quantified the number of cells in the central brain vs. optic lobes of males and females separately. To assess if increases in body size during development might independently affect different regions of the CNS, we quantified the larval ventral nerve cord and central brain separately at all three stages. Together, these data provide the first description of the nervous system of a popular, farmed invertebrate and the first study of brain cell numbers using IF across developmental stages in any insect.</p>
Impact of maternal obesity on the gestational metabolome and infant metabolome, brain, and behavioral development in rhesus macaques
<p>Maternal gestational obesity is associated with elevated risks for neurodevelopmental disorder, including autism spectrum disorder. However, the mechanisms by which maternal adiposity influences fetal developmental programming remain to be elucidated. We aimed to understand the impact of maternal obesity on the metabolism of both pregnant mothers and their offspring, as well as on metabolic, brain, and behavioral development of offspring by utilizing metabolomics, protein, and behavioral assays in a non-human primate model. We found that maternal obesity was associated with elevated inflammation and significant alterations in metabolites of energy metabolism and one-carbon metabolism in maternal plasma and urine, as well as in placenta. Infants born to obese mothers were significantly larger at birth compared to those born to lean mothers. Additionally, they exhibited significantly reduced novelty preference and significant alterations in their emotional response to stress situations. These changes coincided with differences in phosphorylation of enzymes in the brain mTOR signaling pathway between infants born to obese and lean mothers and correlated with the concentration of maternal plasma betaine during pregnancy. In summary, gestational obesity significantly impacted the infant systemic and brain metabolome and adaptive behaviors.</p>
Rapid brain development and reduced neuromodulator titres correlate with host shifts in Rhagoletis pomonella
<p>Host shifts are considered a key generator of insect biodiversity. For insects, adaptation to new host plants often requires changes in larval/pupal development and behavioural preference towards new hosts. Neurochemicals play key roles in both development and behaviour, and therefore provide a potential source for such synchronization. Here, we correlated life history timing, brain development, and corresponding levels of 14 neurochemicals in <em>Rhagoletis pomonella</em> (Diptera: Tephritidae), a species undergoing ecological speciation through an ongoing host shift from hawthorn to apple fruit. These races exhibit differences in pupal diapause timing as well as adult behavioural preference with respect to their hosts. This difference in behavioural preference is coupled with differences in neurophysiological response to host volatiles. We found that apple race pupae exhibited adult brain morphogenesis three weeks faster after an identical simulated winter than the hawthorn race, which correlated with significantly lower titres of several neurochemicals. In some cases, particularly biogenic amines, differences in titres were reflected in the mature adult stage, when host preference is exhibited. In summary, <span>life history timing, neurochemical titre, and brain development </span><span>can be coupled in this speciating system, providing new hypotheses for the origins of new species through host shifts</span>.</p>
Data supporting the manuscript "Human adolescent brain network development is different for paralimbic versus neocortical zones"
<p>This data supports the manuscript "Human adolescent brain network development is different for paralimbic versus neocortical zones" by Dorfschmidt et al. All code used in the analysis can be found here: https://github.com/LenaDorfschmidt/morphometric-similarity-adolescence/</p>
Table 1 in Delphinid brain development from neonate to adulthood with comparisons to other cetaceans and artiodactyls
<p><i>Table 1.</i> Comparison of adult and neonate index of encephalization (EQ) for 15 cetacean (1 mysticete, 14 odontocete) species. EQs were derived from brain and body masses in Table S1.</p><table><thead><tr><th>Family</th><th>Species</th><th>Adult EQ</th><th>Neonate EQ</th></tr></thead><tbody><tr><th>Balaenopteridae</th><td><i>B. physalus</i></td><td>0.495</td><td>2.297</td></tr><tr><th>Delphinidae</th><td><i>C. commersonii</i></td><td>5.149</td><td>7.234</td></tr><tr><th></th><td><i>D. delphis</i></td><td>3.962</td><td>7.801</td></tr><tr><th></th><td><i>G. griseus</i></td><td>4.055</td><td>5.807</td></tr><tr><th></th><td><i>L. acutus</i></td><td>3.805</td><td>6.632</td></tr><tr><th></th><td><i>L. obliquidens</i></td><td>4.635</td><td>8.315</td></tr><tr><th></th><td><i>O. orca</i></td><td>2.425</td><td>8.317</td></tr><tr><th></th><td><i>S. bredanensis</i></td><td>5.633</td><td>8.065</td></tr><tr><th></th><td><i>T. truncatus</i></td><td>3.972</td><td>8.328</td></tr><tr><th>Physeteridae</th><td><i>P. macrocephalus</i></td><td>0.681</td><td>4.402</td></tr><tr><th>Kogiidae</th><td><i>K. breviceps</i></td><td>1.703</td><td>4.767</td></tr><tr><th>Pontoporiidae</th><td><i>P. blainvillei</i></td><td>1.930</td><td>2.571</td></tr><tr><th>Monodontidae</th><td><i>D. leucas</i></td><td>2.643</td><td>5.764</td></tr><tr><th>Phocoenidae</th><td><i>P. phocoena</i></td><td>2.837</td><td>4.406</td></tr><tr><th></th><td><i>P. dalli</i></td><td>2.909</td><td>3.275</td></tr></tbody></table>
A transposase-derived gene responsible for human brain development
<p><span>Vertebrate brain development is associated with prominent neuronal cell death and DNA breaks, but their causes and functions are not well understood. DNA transposable elements and transposase-derived genes could contribute to DNA breaks and somatic genome rearrangements, however their contributions to brain development are largely unknown. PiggyBac Transposable Element Derived 5 (PGBD5) is an evolutionarily conserved vertebrate DNA transposase-derived gene with retained nuclease activity in human cells. Here, we show that PGBD5 contributes to normal brain development in mice and humans, and its deficiency causes disorder of intellectual disability, movement, and seizures. In mice, Pgbd5 is required for the developmental induction of post-mitotic DNA breaks and recurrent somatic brain<em> </em>genome rearrangements. In the cerebral cortex, loss of Pgbd5 leads to aberrant differentiation and gene expression of distinct neuronal populations, including specific types of glutamatergic neurons, which can explain the features of PGBD5 deficiency in humans. Thus, PGBD5 is a transposase-derived gene required for brain development in mammals. </span></p>
Calorie restriction and pravastatin administration during pregnancy in obese rhesus macaques modulates maternal and infant metabolism and infant brain and behavioral development
<p>Maternal obesity has been associated with a higher risk of pregnancy-related complications in mothers and offspring; however, effective interventions have not yet been developed. We tested two common interventions, calorie restriction and pravastatin administration, during pregnancy in a rhesus macaque model with the hypothesis that these interventions would normalize metabolic dysregulation in pregnant mothers leading to an improvement in infant metabolic and cognitive/social development. A total of 19 obese mothers were assigned to either one of the two intervention groups (n=5 for calorie restriction; n=7 for pravastatin) or an obese control group (n=7) with no intervention, and maternal gestational samples and postnatal infant samples were compared with lean control mothers (n=6). Gestational calorie restriction normalized one-carbon metabolism dysregulation in obese mothers but altered energy metabolism in their offspring. Although administration of pravastatin during pregnancy tended to normalize blood cholesterol in the mothers, it potentially impacted the gut microbiome and kidney function of their offspring. In the offspring, both calorie restriction and pravastatin administration during pregnancy tended to normalize the activity of AMPK in the brain at 6 months, and while results of the Visual Paired-Comparison test, which measures infant recognition memory, were not significantly impacted by either of the interventions, gestational pravastatin administration, but not calorie restriction, tended to normalize anxiety assessed by the Human Intruder test. Although the two interventions tested in a non-human primate model led to some improvements in metabolism and/or infant brain development, negative impacts were also found in both mothers and infants. Our study emphasizes the importance of assessing gestational interventions for maternal obesity on both maternal and offspring long-term outcomes.</p>
Targeting Human Milk Fortification to Improve Preterm Infant Growth and Brain Development
ClinicalTrials.gov study NCT03977259. IPD Sharing: NO. Countries: 1. Publications: 1.
Developing Brain, Impulsivity and Compulsivity
ClinicalTrials.gov study NCT04631042. IPD Sharing: YES. Countries: 1. Publications: 3.
Calorie restriction and pravastatin administration during pregnancy in obese rhesus macaques modulates maternal and infant metabolism and infant brain and behavioral development
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Impacts of development and adult sex on brain cell numbers in the Black Soldier Fly, Hermetia illucens L. (Diptera: Stratiomyidae)
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Multimodal 3-D histology atlas volumes and plates for developing human brains
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Impact of maternal obesity on the gestational metabolome and infant metabolome, brain, and behavioral development in rhesus macaques
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Rapid brain development and reduced neuromodulator titres correlate with host shifts in Rhagoletis pomonella
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Sex‐dimorphic effects of biogenesis of lysosome‐related organelles complex‐1 deficiency on mouse perinatal brain development
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Data from: Brain plasticity over the metamorphic boundary: carry-over effect of larval environment on froglet brain development
Brain development shows high plasticity in response to environmental heterogeneity. However, it is unknown how environmental variation during development may affect brain architecture across life history switch points in species with complex life cycles. Previously, we showed that predation and competition affect brain development in common frog (Rana temporaria) tadpoles. Here, we studied if larval environment had carry-over effects in brains of metamorphs. Tadpoles grown at high density had large optic tecta at metamorphosis, while tadpoles grown under predation risk had small diencephala. We found that larval density had a carry-over effect on froglet optic tectum size, while the effect of larval predation risk had vanished by metamorphosis. We discuss the possibility that the observed changes may be adaptive, reflecting the needs of an organism in given environmental and developmental contexts.
Insecticide exposure during brood or early-adult development reduces brain growth and impairs adult learning in bumblebees
<p>For social bees, an understudied step in evaluating pesticide risk is how contaminated food entering colonies affects residing offspring development and maturation. For instance, neurotoxic insecticide compounds in food could affect central nervous system development predisposing individuals to become poorer task performers later-in-life. Studying bumblebee colonies provisioned with neonicotinoid spiked nectar substitute, we measured brain volume and learning behaviour of 3 or 12-day old adults that had experienced in-hive exposure during brood and/or early-stage adult development. Micro-computed tomography (µCT) scanning and segmentation of multiple brain neuropils showed exposure during either developmental stage caused reduced mushroom body calycal growth relative to unexposed workers. Associated with this, was a lower probability of responding to a sucrose reward and lower learning performance in an olfactory conditioning test. Whilst calycal volume of control workers positively correlated with learning score, this relationship was absent for exposed workers indicating neuropil functional impairment. Comparison of 3 and 12-day adults exposed during brood development showed a similar degree of reduced calycal volume and impaired behaviour highlighting lasting and irrecoverable effects from exposure despite no adult exposure. Our findings help explain how the onset of pesticide exposure to whole colonies can lead to lag-effects on growth and resultant dysfunction.</p>
Data from: Sociosexual and communication deficits after traumatic injury to the developing murine brain
Despite the life-long implications of social and communication dysfunction after pediatric traumatic brain injury, there is a poor understanding of these deficits in terms of their developmental trajectory and underlying mechanisms. In a well-characterized murine model of pediatric brain injury, we recently demonstrated that pronounced deficits in social interactions emerge across maturation to adulthood after injury at postnatal day (p) 21, approximating a toddler-aged child. Extending these findings, we here hypothesized that these social deficits are dependent upon brain maturation at the time of injury, and coincide with abnormal sociosexual behaviors and communication. Age-dependent vulnerability of the developing brain to social deficits was addressed by comparing behavioral and neuroanatomical outcomes in mice injured at either a pediatric age (p21) or during adolescence (p35). Sociosexual behaviors including social investigation and mounting were evaluated in a resident-intruder paradigm at adulthood. These outcomes were complemented by assays of urine scent marking and ultrasonic vocalizations as indices of social communication. We provide evidence of sociosexual deficits after brain injury at p21, which manifest as reduced mounting behavior and scent marking towards an unfamiliar female at adulthood. In contrast, with the exception of the loss of social recognition in a three-chamber social approach task, mice that received TBI at adolescence were remarkably resilient to social deficits at adulthood. Increased emission of ultrasonic vocalizations (USVs) as well as preferential emission of high frequency USVs after injury was dependent upon both the stimulus and prior social experience. Contrary to the hypothesis that changes in white matter volume may underlie social dysfunction, injury at both p21 and p35 resulted in a similar degree of atrophy of the corpus callosum by adulthood. However, loss of hippocampal tissue was greater after p21 compared to p35 injury, suggesting that a longer period of lesion progression or differences in the kinetics of secondary pathogenesis after p21 injury may contribute to observed behavioral differences. Together, these findings indicate vulnerability of the developing brain to social dysfunction, and suggest that a younger age-at-insult results in poorer social and sociosexual outcomes.
Data from: Light-at-night exposure affects brain development through pineal allopregnanolone-dependent mechanisms
The molecular mechanisms by which environmental light conditions affect cerebellar development are incompletely understood. We showed that circadian disruption by light-at-night induced Purkinje cell death through pineal allopregnanolone (ALLO) activity during early life in chicks. Light-at-night caused the loss of diurnal variation of pineal ALLO synthesis during early life and led to cerebellar Purkinje cell death, which was suppressed by a daily injection of ALLO. The loss of diurnal variation of pineal ALLO synthesis induced not only reduction in pituitary adenylate cyclase-activating polypeptide (PACAP), a neuroprotective hormone, but also transcriptional repression of the cerebellar Adcyap1 gene that produces PACAP, with subsequent Purkinje cell death. Taken together, pineal ALLO mediated the effect of light on early cerebellar development in chicks.
Severe hypoxia exposure inhibits larval brain development but does not affect the capacity to mount a cortisol stress response in zebrafish
<p>Fish nursery habitats are increasingly hypoxic and the brain is recognized as highly hypoxia-sensitive, yet there is a lack of information on the effects of hypoxia on the development and function of the larval fish brain. Here, we tested the hypothesis that by inhibiting brain development, larval exposure to severe hypoxia has persistent functional effects on the cortisol stress response in zebrafish (<i>Danio rerio</i>). Exposing 5 days post-fertilization (dpf) larvae to 10% dissolved O<sub>2</sub> (DO) for 16 h only marginally reduced survival, but it decreased forebrain neural proliferation by 55%, and reduced the expression of <i>neurod1</i>, <i>gfap,</i> and <i>mbpa, </i>markers of determined neurons, glia, and oligodendrocytes, respectively. The 5 dpf hypoxic exposure also elicited transient increases in whole body cortisol and in <i>crf</i>, <i>uts1</i>, and <i>hsd20b2</i> expression, key regulators of the endocrine stress response. Hypoxia exposure at 5 dpf also inhibited the cortisol stress response to hypoxia in 10 dpf larvae and increased hypoxia tolerance. However, 10% DO exposure at 5 dpf for 16h did not affect the cortisol stress response to a novel stressor in 10 dpf larvae or the cortisol stress response to hypoxia in adult fish. Therefore, while larval exposure to severe hypoxia can inhibit brain development, it also increases hypoxia tolerance. These effects may transiently reduce the impact of hypoxia on the cortisol stress response but not its functional capacity to respond to novel stressors. We conclude that the larval cortisol stress response in zebrafish has a high capacity to cope with severe hypoxia-induced neurogenic impairment.</p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
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OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.