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Updated: Apr 22, 2026
Neurodevelopmental Reflex Testing in Neonatal Rat Pups
Published on: April 24, 2017
Neonatal dexamethasone accelerates spreading depression in the rat, and antioxidant vitamins counteract this effect
Andréia Albuquerque Cunha Lopes-de-Morais1, Rosângela Figueiredo Mendes-da-Silva1, Eryka Maria dos-Santos1
1Departamento de Nutrição, Universidade Federal de Pernambuco, Recife, PE 50670-901, Brazil.
Insights
Neonatal dexamethasone (Dex) treatment increased cortical spreading depression (CSD) velocity in rats. Co-administration of vitamins C and E with Dex reduced this adverse brain effect, suggesting a potential therapeutic strategy.
Area of Science:
- Neuroscience
- Developmental Biology
- Pharmacology
Background:
- Dexamethasone (Dex) is used to treat chronic lung disease in preterm infants.
- Neonatal Dex administration may lead to adverse effects on the developing brain.
- Cortical spreading depression (CSD) is a neurophysiological phenomenon sensitive to brain conditions.
Purpose of the Study:
- To evaluate the impact of neonatal dexamethasone on cortical spreading depression (CSD) propagation.
- To investigate the neuroprotective potential of vitamins C and E against dexamethasone-induced CSD alterations.
Main Methods:
- Wistar rats were administered dexamethasone, vehicle, or vitamins C and E, with or without dexamethasone, during the neonatal period (postnatal days 1-3 or 1-6).
- CSD velocities were measured in adulthood (postnatal days 60-70) using electrocorticography.
- P-wave amplitude and duration, and CSD-induced ECoG potentiation were also analyzed.
Main Results:
- Neonatal dexamethasone treatment significantly increased CSD velocities compared to control groups (p<0.05).
- Co-administration of vitamins C and E with dexamethasone (DexCE group) antagonized the increased CSD velocity.
- No significant intergroup differences were found in P-wave parameters or CSD-induced ECoG potentiation.
Conclusions:
- Neonatal dexamethasone exposure alters cortical spreading depression propagation in developing brains.
- Antioxidant vitamins C and E demonstrate a protective effect against dexamethasone-induced neurophysiological changes.
- Combined administration of dexamethasone with antioxidant vitamins may represent a viable strategy to mitigate dexamethasone's adverse brain effects.
Abstract:
The use of dexamethasone (Dex) to treat chronic lung disease in preterm infants may produce adverse effects in the developing brain. Here, we evaluated the effects of neonatal Dex on the propagation of cortical spreading depression (CSD), and tested the action of vitamins C and E against the effect of Dex. Five groups of Wistar rats received, respectively: [1] no treatment (Naïve); [2] Vehicle (V); [3] tapering doses of Dex (Dex; 0.5mg/kg, 0.3mg/kg, and 0.1mg/kg) on postnatal day (PND) 1-3; [4] Dex plus 200mg/kg vitamin C and 100mg/kg vitamin E (DexCE); [5] only vitamins C and E (CE). Vehicle and vitamins were administered on PND 1-6. CSD was recorded after the pups reached maturity (PND 60-70). The Dex-treated group presented with higher CSD velocities (mean values ± SD, in mm/min: 4.14 ± 0.22, n=10) compared with the control groups (Naïve: 3.52 ± 0.13, n=8; V: 3.57 ± 0.18, n=10; CE: 3.51 ± 0.24, n=10; p<0.05 for all). Vitamins C and E antagonized this effect (DexCE group; CSD velocity: 3.43 ± 0.12, n=9). No intergroup difference was observed concerning P-wave amplitude and duration. In all groups, after the cortex underwent CSD, the electrocorticogram (ECoG) amplitude increased approximately 50% compared with the baseline amplitude for the same animal (CSD-induced ECoG potentiation); however, no intergroup difference was observed. Data suggest that coadministration of antioxidant vitamins with Dex may be a helpful therapeutic strategy to reduce brain adverse effects of dexamethasone.
