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Brain development in rodents and humans: Identifying benchmarks of maturation and vulnerability to injury across species
Open accessAbstract
Hypoxic-ischemic and traumatic brain injuries are leading causes of long-term mortality and disability in infants and children. Although several preclinical models using rodents of different ages have been developed, species differences in the timing of key brain maturation events can render comparisons of vulnerability and regenerative capacities difficult to interpret. Traditional models of developmental brain injury have utilized rodents at postnatal day 7-10 as being roughly equivalent to a term human infant, based historically on the measurement of post-mortem brain weights during the 1970s. Here we will examine fundamental brain development processes that occur in both rodents and humans, to delineate a comparable time course of postnatal brain development across species. We consider the timing of neurogenesis, synaptogenesis, gliogenesis, oligodendrocyte maturation and age-dependent behaviors that coincide with developmentally regulated molecular and biochemical changes. In general, while the time scale is considerably different, the sequence of key events in brain maturation is largely consistent between humans and rodents. Further, there are distinct parallels in regional vulnerability as well as functional consequences in response to brain injuries. With a focus on developmental hypoxic-ischemic encephalopathy and traumatic brain injury, this review offers guidelines for researchers when considering the most appropriate rodent age for the developmental stage or process of interest to approximate human brain development.
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“the CNS exhibits regionally and temporally distinct patterns of vulnerability to various diseases and insults (Figure 2) (Kessler et al., 2007; Lee et al., 2014; Semple et al., 2013; Tebbenkamp et al., 2014).”
From The Cellular and Molecular Landscapes of the Developing Human Central Nervous System (2016) · cites this paper as Semple et al., 2013
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“development of the human brain is protracted compared to other species (Clancy et al., 2001; Miller et al, 2012; Semple et al., 2013), so despite having a more “mature” brain at birth compared to rats, vulnerability to insult remains.”
From The effects of early life stress on reward processing (2018) · cites this paper as Semple et al., 2013
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“the age at which maternal separation occurs in most animal experiments corresponds to a gestational age in humans, at least in terms of some aspects of brain development (Semple et al., 2013).”
From The effects of early life stress on reward processing (2018) · cites this paper as Semple et al., 2013
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“Interestingly, the distinct neural plasticity during development can lead to cortical adaptation with very specific regionally altered cortical representation fields (436, 437) and be potentially protecting from the specific sensory processing of different ELS/CT (417).”
Background
Metadata
- Authors
- Semple, B. D., Blomgren, K., Gimlin, K., Ferriero, D. M., & Noble-Haeusslein, L. J.
- Affiliations
- University of California, San Francisco (US)
- Karolinska Institutet (SE)
- Corresponding author
- Semple, Bridgette D.
- Venue
- Progress in Neurobiology
- Publisher
- Elsevier BV
- Published
- 2013-07
- Volume
- 106-107
- Pages
- 1-16
- ISSN
- 0301-0082 (ISSN-L)
- PMC
- PMC3737272
- OpenAlex
- W2027917639
- Cited by
- 2,132
- References
- 252
- Citations by year
- 2026: 156 · 2025: 210 · 2024: 211 · 2023: 212 · 2022: 219 · 2021: 241 · 2020: 213 · 2019: 203 · 2018: 164 · 2017: 128 · 2016: 80 · 2015: 51 · 2014: 30 · 2013: 9
- FWCI
- 8.02
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Progress in Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health (5r01ns077767-02)
- National Institute of Neurological Disorders and Stroke (#R01NS077767, R01NS050159, NS077767)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- brain development, developmental brain injury, hypoxic-ischemic encephalopathy, traumatic brain injury, rodent models, postnatal development, neurogenesis, synaptogenesis, gliogenesis, oligodendrocyte maturation, species differences, developmental vulnerability, preclinical models
- MeSH terms
- Animals, Brain, Brain Injuries, Humans, Oligodendroglia, Rodentia, Hypoxia-Ischemia, Brain, Neurogenesis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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