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Mol Neurobiol. 2018 May;55(5):3627-3641. doi: 10.1007/s12035-017-0604-5. Epub 2017 May 18.

Prenatal and Early Postnatal Environmental Enrichment Reduce Acute Cell Death and Prevent Neurodevelopment and Memory Impairments in Rats Submitted to Neonatal Hypoxia Ischemia.

Author information

1
Post-graduation Program of Physiology, Institute of Health Science, Universidade Federal do Rio Grande do Sul (UFRGS), Rua Ramiro Barcelos 2600, anexo, Porto Alegre, RS, CEP 90035-003, Brazil. luzeled67@gmail.com.
2
Department of Biochemistry, Institute of Health Science, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil.
3
Post-graduation Program of Physiology, Institute of Health Science, Universidade Federal do Rio Grande do Sul (UFRGS), Rua Ramiro Barcelos 2600, anexo, Porto Alegre, RS, CEP 90035-003, Brazil.
4
Neurorehabilitation and Neural Repair Research Group, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, RS, Brazil.
5
Post-graduation Program of Neuroscience, Institute of Health Science|, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil.
6
Rehabilitation Sciences Graduate Program, Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA), Porto Alegre, Brazil.

Abstract

Environmental enrichment (EE) is an experimental strategy to attenuate the negative effects of different neurological conditions including neonatal hypoxia ischemia encephalopathy (HIE). The aim of the present study was to investigate the influence of prenatal and early postnatal EE in animals submitted to neonatal HIE model at postnatal day (PND) 3. Wistar rats were housed in EE or standard conditions (SC) during pregnancy and lactation periods. Pups of both sexes were assigned to one of four experimental groups, considering the early environmental conditions and the injury: SC-Sham, SC-HIE, EE-sham, and EE-HIE. The offspring were euthanized at two different time points: 48 h after HIE for biochemical analyses or at PND 67 for histological analyses. Behavioral tests were performed at PND 7, 14, 21, and 60. Offspring from EE mothers had better performance in neurodevelopmental and spatial memory tests when compared to the SC groups. HIE animals showed a reduction of IGF-1 and VEGF in the parietal cortex, but no differences in BDNF and TrkB levels were found. EE-HIE animals showed reduction in cell death, lower astrocyte reactivity, and an increase in AKTp levels in the hippocampus and parietal cortex. In addition, the EE was also able to prevent the hippocampus tissue loss. Altogether, present findings point to the protective potential of the prenatal and early postnatal EE in attenuating molecular and histological damage, as well as the neurodevelopmental impairments and the cognitive deficit, caused by HIE insult at PND 3.

KEYWORDS:

Cell death; Environmental stimulation; Gestation; Memory; Neurodevelopment; Pre-weaning period; Prematurity

PMID:
28523564
DOI:
10.1007/s12035-017-0604-5
[Indexed for MEDLINE]

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