The postnatal day (P) 3 rat model of hypoxic-ischemic (HI) brain injury provides valuable information regarding the cellular response to HI injury in a very immature brain. Our present study is the first to examine growth, metabolic, and behavioral outcomes following a P3 HI brain injury. Rats were injured by cauterizing the right common carotid, and exposure to 8% oxygen for 1.5h. Control rats received sham surgery and exposure to 1.5h of room air. One cohort of rats was examined for growth patterns through P33, evaluated using a battery of tests focused on early postnatal feeding behaviors, and studied using the open field paradigm during the early postnatal and postweaning periods. Another cohort of rats was used to examine metabolic parameters using indirect calorimetry. Significant growth deficits emerged in injured rats during the second postnatal week. No significant differences between groups were noted in the expression of feeding-related behaviors or in metabolic parameters between groups. However, we did observe significant associations between feeding-related behaviors and P14 growth parameters in injured rats. In the open field assessment, HI rats showed increased circling and supination behaviors only during the early postnatal period. Our data reveal that P3 HI brain injury results in generalized growth deficits that persist through postweaning. Analyses suggest that alterations in feeding-related behaviors contribute to growth deficits following a P3 HI brain injury.
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http://dx.doi.org/10.1016/j.bbr.2009.03.043 | DOI Listing |
Nat Commun
January 2025
Unit on the Development of Neurodegeneration, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
Traumatic brain injury (TBI) is a risk factor for neurodegeneration, however little is known about how this kind of injury alters neuron subtypes. In this study, we follow neuronal populations over time after a single mild TBI (mTBI) to assess long ranging consequences of injury at the level of single, transcriptionally defined neuronal classes. We find that the stress-responsive Activating Transcription Factor 3 (ATF3) defines a population of cortical neurons after mTBI.
View Article and Find Full Text PDFeNeuro
January 2025
Department of Biology, University of Ottawa, Ottawa, ON K1N 6N5, Canada.
Axons in the mammalian brain show significant diversity in myelination motifs, displaying spatial heterogeneity in sheathing along individual axons and across brain regions. However, its impact on neural signaling and susceptibility to injury remains poorly understood. To address this, we leveraged cable theory and developed model axons replicating the myelin sheath distributions observed experimentally in different regions of the mouse central nervous system.
View Article and Find Full Text PDFBrain Behav Immun
January 2025
Laboratories of Neuroimmunology, Department of Symptom Research, University of Texas MD Anderson Cancer Center, Houston, USA. Electronic address:
Preclinical and clinical studies have established that autoreactive immunoglobulin G (IgG) can drive neuropathic pain. We recently demonstrated that sciatic nerve chronic constriction injury (CCI) in male and female mice results in the production of pronociceptive IgG, which accumulates around the lumbar region, including within the dorsal root ganglia (DRG) and spinal cord, facilitating the development of neuropathic pain. These data raise the intriguing possibility that neuropathic pain may be alleviated by reducing the accumulation of IgG.
View Article and Find Full Text PDFStem Cell Rev Rep
January 2025
Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China.
Background: The hypobaric hypoxic atmosphere can cause adverse reactions or sickness. The purpose of this study was to explore the preventive effect and mechanism of human umbilical cord mesenchymal stem cells (hUC-MSCs) on acute pathological injury in mice exposed to high-altitude.
Methods: We pretreated C57BL/6 mice with hUC-MSCs via the tail vein injection, and then the mice were subjected to hypobaric hypoxic conditions for five days.
J Biophotonics
January 2025
Britton Chance Center for Biomedical Photonics-MoE Key Laboratory for Biomedical Photonics, Huazhong University of Science and Technology, Wuhan, China.
Diabetes mellitus (DM), a chronic metabolic disorder that adversely affects the blood-brain barrier (BBB) and microglial function in the central nervous system (CNS), contributing to neuronal damage and neurodegenerative diseases. However, the underlying molecular mechanisms linking diabetes to BBB dysfunction and microglial dysregulation remain poorly understood. Here, we assessed the impacts of diabetes on BBB and microglial reactivity and investigated its mechanisms.
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