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Neurobehavioral Assessments in a Mouse Model of Neonatal Hypoxic-ischemic Brain Injury
Published on: November 24, 2017
Growth deficits in a postnatal day 3 rat model of hypoxic-ischemic brain injury
Wei-Cheng Tai1, Kathleen A Burke, Jesus F Dominguez
1Center for Premature Infant Health and Development, Keck School of Medicine, University of Southern California, Los Angeles, CA 90089, USA.
Insights
Hypoxic-ischemic (HI) brain injury in newborn rats causes lasting growth deficits. Altered feeding behaviors appear to contribute to these growth problems in young HI brain injury models.
Area of Science:
- Neuroscience
- Developmental Biology
- Pediatric Research
Background:
- The postnatal day 3 (P3) rat model simulates immature brain injury.
- Hypoxic-ischemic (HI) brain injury impacts developing neural systems.
- Understanding early brain injury is critical for pediatric outcomes.
Purpose of the Study:
- To investigate growth, metabolic, and behavioral effects of P3 HI brain injury.
- To establish long-term consequences of early-life brain damage.
- To explore the relationship between feeding behaviors and growth deficits.
Main Methods:
- P3 rats underwent HI brain injury (carotid cauterization, 8% oxygen) or sham surgery.
- Growth was monitored until P33.
- Behavioral tests (feeding, open field) and indirect calorimetry were employed.
Main Results:
- HI rats exhibited significant growth deficits from the second postnatal week, persisting post-weaning.
- No significant differences in feeding behaviors or metabolic parameters were observed between groups.
- Early HI injury was associated with increased circling and supination in the open field test.
Conclusions:
- P3 HI brain injury induces persistent, generalized growth deficits.
- Altered feeding behaviors are implicated as a contributing factor to growth impairments.
- This model offers insights into cellular responses and long-term outcomes of immature brain injury.
Abstract:
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.
