Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 757 - 766 |
| Number of pages | 10 |
| Journal | International Journal of Developmental Neuroscience |
| Volume | 29 |
| Issue number | 7 |
| DOIs | |
| Publication status | Published - 2011 |
Cite this
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Effects of birth asphyxia on neonatal hippocampal structure and function in the spiny mouse. / Fleiss, Bobbi; Coleman, Harold; Zakhem, Margie Esmeralda; Ireland, Zoe; Walker, David; Parkington, Helena.
In: International Journal of Developmental Neuroscience, Vol. 29, No. 7, 2011, p. 757 - 766.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - Effects of birth asphyxia on neonatal hippocampal structure and function in the spiny mouse
AU - Fleiss, Bobbi
AU - Coleman, Harold
AU - Zakhem, Margie Esmeralda
AU - Ireland, Zoe
AU - Walker, David
AU - Parkington, Helena
PY - 2011
Y1 - 2011
N2 - Studies of human neonates, and in animal experiments, suggest that birth asphyxia results in functional compromise of the hippocampus, even when structural damage is not observable or resolves in early postnatal life. The aim of this study was to determine if changes in hippocampal function occur in a model of birth asphyxia in the precocial spiny mouse where it is reported there is no major lesion or infarct. Further, to assess if, as in human infants, this functional deficit has a sex-dependent component. At 37 days gestation (term=39 days) spiny mice fetuses were either delivered immediately by caesarean section (control group) or exposed to 7.5min of in utero asphyxia causing systemic acidosis and hypoxia. At 5 days of age hippocampal function was assessed ex vivo in brain slices, or brains were collected for examination of structure or protein expression. This model of birth asphyxia did not cause infarct or cystic lesion in the postnatal day 5 (P5) hippocampus, and the number of proliferating or pyknotic cells in the hippocampus was unchanged, although neuronal density in the CA1 and CA3 was increased. Protein expression of synaptophysin, brain-derived neurotrophic factor (BDNF), and the inositol trisphosphate receptor 1 (IP(3)R1) were all significantly increased after birth asphyxia, while long-term potentiation (LTP), paired pulse facilitation (PPF), and post-tetanic potentiation (PTP) were all reduced at P5 by birth asphyxia. In control P5 pups, PPF and synaptic fatigue were greater in female compared to male pups, and after birth asphyxia PPF and synaptic fatigue were reduced to a greater extent in female vs. male pups. In contrast, the asphyxia-induced increase in synaptophysin expression and neuronal...
AB - Studies of human neonates, and in animal experiments, suggest that birth asphyxia results in functional compromise of the hippocampus, even when structural damage is not observable or resolves in early postnatal life. The aim of this study was to determine if changes in hippocampal function occur in a model of birth asphyxia in the precocial spiny mouse where it is reported there is no major lesion or infarct. Further, to assess if, as in human infants, this functional deficit has a sex-dependent component. At 37 days gestation (term=39 days) spiny mice fetuses were either delivered immediately by caesarean section (control group) or exposed to 7.5min of in utero asphyxia causing systemic acidosis and hypoxia. At 5 days of age hippocampal function was assessed ex vivo in brain slices, or brains were collected for examination of structure or protein expression. This model of birth asphyxia did not cause infarct or cystic lesion in the postnatal day 5 (P5) hippocampus, and the number of proliferating or pyknotic cells in the hippocampus was unchanged, although neuronal density in the CA1 and CA3 was increased. Protein expression of synaptophysin, brain-derived neurotrophic factor (BDNF), and the inositol trisphosphate receptor 1 (IP(3)R1) were all significantly increased after birth asphyxia, while long-term potentiation (LTP), paired pulse facilitation (PPF), and post-tetanic potentiation (PTP) were all reduced at P5 by birth asphyxia. In control P5 pups, PPF and synaptic fatigue were greater in female compared to male pups, and after birth asphyxia PPF and synaptic fatigue were reduced to a greater extent in female vs. male pups. In contrast, the asphyxia-induced increase in synaptophysin expression and neuronal...
UR - http://www.ncbi.nlm.nih.gov/pubmed/21641987
U2 - 10.1016/j.ijdevneu.2011.05.006
DO - 10.1016/j.ijdevneu.2011.05.006
M3 - Article
VL - 29
SP - 757
EP - 766
JO - International Journal of Developmental Neuroscience
JF - International Journal of Developmental Neuroscience
SN - 0736-5748
IS - 7
ER -