Table I.
A summary of results of publications in this review
| Authors | Year | Major outcomes of uterine artery ligation |
|---|---|---|
| Reid et al.1 | 2012 | Oligodendrocyte differentiation was delayed until adulthood |
| MBP4 expression was upregulated in early life but normalized in adulthood | ||
| Adult females demonstrated behavioural deficits | ||
| Oxidative stress resulted in BMP4 upregulation and subsequent delayed myelination | ||
| Delcour et al.9 | 2012 | There was white matter damage and deficits in myelination |
| Astrogliosis, neuronal cell loss, and axonal degeneration occurred within white matter | ||
| There was normal neuronal density within the hippocampus and cingulate cortex | ||
| There were also behavioural deficits in locomotor and sensorimotor function, short-term memory, information coding, and sensory gating function | ||
| Spatial and working memory were spared | ||
| Rehn et al.10 | 2004 | Brain weight and basal ganglia volume were decreased |
| Lateral ventricles were enlarged | ||
| Catecholamine expression was unaffected | ||
| Prepulse inhibition was reduced into adulthood | ||
| Delcour et al.11 | 2012 | There was white matter damage within the corpus callosum, brainstem, hippocampus, and somatosensory cortex |
| But white matter was spared within the motor cortex | ||
| Motor maps were abnormal within the somatosensory cortex but were spared within the motor cortex | ||
| Spasticity and hyperactivity were present | ||
| There were short-term memory deficits | ||
| Mallard et al.12 | 2000 | Neuronal density within CA1 and the cerebellum was reduced |
| Volume of cerebellar white matter was reduced | ||
| Fung et al.14 | 2012 | There were reduced neuronal density and immature oligodendrocytes with astrogliosis in the hippocampus |
| ErbB-R expression was increased within the hippocampus | ||
| Tolcos et al.18 | 2011 | There was reduction in white matter in fetuses but not into adulthood |
| Myelinating oligodendrocytes (MBP, MAG, PLP) were reduced but normalized postnatally | ||
| Turner and Trudinger19 | 2009 | Body weight was reduced |
| There was a relative sparing of brain size | ||
| Dieni and Rees20 | 2005 | BDNF expression was reduced and TrkB expression was increased in the hippocampus |
| BDNF and TrkB expression in cerebellum were unaffected | ||
| Catteau et al.21 | 2011 | Birthweight was reduced |
| There was aberrant expression of vascular endothelial growth factor and NMDA receptors | ||
| Olivier et al.22 | 2005 | There were increased numbers of microglial cells and astrogliosis within the cingulate cortex and internal capsule |
| There was preoligodendrocyte apoptosis and subsequent scarcity | ||
| Hypomyelination was present until adulthood | ||
| Tashima et al.24 | 2001 | There was abnormal neuronal migration within the cerebral cortex |
| There were locomotor deficits in adult male rats but not in female rats | ||
| Mallard et al.25 | 1999 | Cerebral ventricles were enlarged |
| The cerebral cortex and hippocampal size were reduced | ||
| Olivier27 | 2007 | There was white matter damage, increased microglia, and astrogliosis |
| There was a reduction in preoligodendrocytes and myelination delay | ||
| Uysal29 | 2008 | Inducible NOS and p53 within the cortex were increased |
| Inducible NOS and endothelial NOS were increased and Bcl-2 expression decreased within the ventricular zone | ||
| Lane et al.30 | 2001 | Bcl-2 expression was decreased within the cortex |
| Bcl-2-associated X protein and caspase-3 activity were unaffected | ||
| Ke et al.31 | 2005 | There was increased p53 expression |
| Expression of murine double minute 2 was reduced | ||
| Olivier et al.37 | 2009 | Microglial activation and astrogliosis were present |
| There was a reduction in and delayed maturation of oligodendrocytes | ||
| Tolcos and Rees38 | 1997 | There were increased astrocyte populations within the vagus, nucleus tractus solitarius, and brain stem |
| Nitsos and Rees39 | 1990 | Hypomyelination was present within the cerebral cortex, corpus callosum, and cerebellum |
| There was astrocytosis within the cerebral cortex but not the cerebellum | ||
| Delayed myelination and hypomyelination were present but the total neuronal fibre count was unaffected | ||
| Tatli et al.42 | 2007 | There was lipid peroxidation and oxidative damage within the cerebellum and cerebral cortex |
| Dieni and Rees45 | 2003 | Dendritic branching patterns were reduced and abnormal within the hippocampus |
| Nishigori et al.46 | 2008 | There was abnormal expression of BDNF and TrkB throughout the brain |
| Schober et al.49 | 2009 | The hippocampi of males had a reduced NR1 expression and NR2A:NR2B ratio |
| There was reduced MBP within the hippocampus | ||
| O'Grady et al.61 | 2010 | There was an increased level of serum testosterone and reduced levels of hippocampal aromatase expression in males |
BDNF, brain-derived neurotrophic factor; BMP, bone morphogenetic protein; MAG, myelin-associated glycoprotein; MBP, myelin basic protein; NMDA, N-methyl-D-aspartate; NOS, Nitric oxide synthase; PLP, proteolipid protein; TrkB, tyrosine kinase receptor.