Loading…
Oligodendrocytes Death Induced Sensorimotor and Cognitive Deficit in N-nitro-l-arginine methyl Rat Model of Pre-eclampsia
Pre-eclampsia (PE) is a pregnancy complicated syndrome that affects multiple organs including the brain that continue post- delivery in both mother and the offspring. We evaluated the expression of oligodendrocytes in the brain of PE rat model through development as well as the cognitive changes and...
Saved in:
Published in: | Neurochemical research 2020-04, Vol.45 (4), p.902-914 |
---|---|
Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Pre-eclampsia (PE) is a pregnancy complicated syndrome that affects multiple organs including the brain that continue post- delivery in both mother and the offspring. We evaluated the expression of oligodendrocytes in the brain of PE rat model through development as well as the cognitive changes and other behavioural modifications that may occur later in the life of offspring of PE-like rat model. Pregnant rats divided into early-onset and late-onset groups were administered with N-nitro-
l
-arginine methyl (
l
-NAME) through drinking water at gestational days (GD) 8–17. Rats were allowed free access to water throughout the pregnancy. At GD 19, post-natal day (PND) 1 and 60, rats were sacrificed and brain excised for further analysis. The offspring were subjected to behavioural studies for cognitive and sensorimotor impairments before sacrificed at PND 60. Results showed significant down-regulation in the expression of OLIG2 in PE at GD 19 brain which persists till PND 60. Likewise, there was a significant increase in the latency to locate the platform in Morris water maze, time to traverse the balance beam and reduced hanging time on the wire test between the control and the PE treated. PE could lead to impaired neuronal signalling through demyelination which may contributes significantly to long-term sensorimotor and cognitive deficit. |
---|---|
ISSN: | 0364-3190 1573-6903 |
DOI: | 10.1007/s11064-020-02969-5 |