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Updated: Jun 8, 2026
A Battery of Motor Tests in a Neonatal Mouse Model of Cerebral Palsy
Published on: November 3, 2016
Neonatal stroke in mice causes long-term changes in neuronal Notch-2 expression that may contribute to prolonged
Lavinia Albéri1, Zhikai Chi, Shilpa D Kadam
1Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. lavinia.alberi@unifr.ch
Background And Purpose:
Notch receptors (1-4) are membrane proteins that, on ligand stilumation, release their cytoplasmic domains to serve as transcription factors. Notch-2 promotes proliferation both during development and cancer, but its role in response to ischemic injury is less well understood. The purpose of this study was to understand whether Notch-2 is induced after neonatal stroke and to investigate its functional relevance.
Methods:
P12 CD1 mice were subjected to permanent unilateral (right-sided) double ligation of the common carotid artery.
Results:
Neonatal ischemia induces a progressive brain injury with prolonged apoptosis and Notch-2 up-regulation. Notch-2 expression was induced shortly after injury in hippocampal areas with elevated c-fos activation and increased cell death. Long-term induction of Notch-2 also occurred in CA1 and CA3 in and around areas of cell death, and had a distinct pattern of expression as compared to Notch-1. In vitro oxygen glucose deprivation treatment showed a similar increase in Notch-2 in apoptotic cells. In vitro gain of function experiments, using an active form of Notch-2, show that Notch-2 induction is neurotoxic to a comparable extent as oxygen glucose deprivation treatment.
Conclusions:
These results suggest that Notch-2 up-regulation after neonatal ischemia is detrimental to neuronal survival.
