Dendrimer-Based Postnatal Therapy for Neuroinflammation and Cerebral Palsy in a Rabbit Model

2012 ◽  
Vol 2012 ◽  
pp. 180-181
Author(s):  
H. Christou
Keyword(s):  
Cerebral Palsy ◽  
Rabbit Model

scholarly journals Magnitude of [11C]PK11195 Binding Is Related to Severity of Motor Deficits in a Rabbit Model of Cerebral Palsy Induced by Intrauterine Endotoxin Exposure

2011 ◽  
Vol 33 (3-4) ◽  
pp. 231-240 ◽  
Author(s):  
Sujatha Kannan ◽  
Fadoua Saadani-Makki ◽  
Bindu Balakrishnan ◽  
Pulak Chakraborty ◽  
James Janisse ◽  
...  
Keyword(s):  
Cerebral Palsy ◽  
Rabbit Model ◽  
Motor Deficits ◽  
Endotoxin Exposure

scholarly journals Maternal Inflammation Results in Altered Tryptophan Metabolism in Rabbit Placenta and Fetal Brain

2017 ◽  
Vol 39 (5) ◽  
pp. 399-412 ◽  
Author(s):  
Monica Williams ◽  
Zhi Zhang ◽  
Elizabeth Nance ◽  
Julia L. Drewes ◽  
Wojciech G. Lesniak ◽  
...  
Keyword(s):  
Cerebral Palsy ◽  
Microglial Activation ◽  
Rabbit Model ◽  
Fetal Brain ◽  
Kynurenine Pathway ◽  
Tryptophan Metabolism ◽  
Maternal Inflammation ◽  
Newborn Brain ◽  
Tryptophan Pathway ◽  
Tryptophan Metabolites

Maternal inflammation has been linked to neurodevelopmental and neuropsychiatric disorders such as cerebral palsy, schizophrenia, and autism. We had previously shown that intrauterine inflammation resulted in a decrease in serotonin, one of the tryptophan metabolites, and a decrease in serotonin fibers in the sensory cortex of newborns in a rabbit model of cerebral palsy. In this study, we hypothesized that maternal inflammation results in alterations in tryptophan pathway enzymes and metabolites in the placenta and fetal brain. We found that intrauterine endotoxin administration at gestational day 28 (G28) resulted in a significant upregulation of indoleamine 2,3-dioxygenase (IDO) in both the placenta and fetal brain at G29 (24 h after treatment). This endotoxin-mediated IDO induction was also associated with intense microglial activation, an increase in interferon gamma expression, and increases in kynurenine and the kynurenine pathway metabolites kynurenine acid and quinolinic acid, as well as a significant decrease in 5-hydroxyindole acetic acid (a precursor of serotonin) levels in the periventricular region of the fetal brain. These results indicate that maternal inflammation shunts tryptophan metabolism away from the serotonin to the kynurenine pathway, which may lead to excitotoxic injury along with impaired development of serotonin-mediated thalamocortical fibers in the newborn brain. These findings provide new targets for prevention and treatment of maternal inflammation-induced fetal and neonatal brain injury leading to neurodevelopmental disorders such as cerebral palsy and autism.

scholarly journals Intrauterine administration of endotoxin leads to motor deficits in a rabbit model: a link between prenatal infection and cerebral palsy

2008 ◽  
Vol 199 (6) ◽  
pp. 651.e1-651.e7 ◽  
Author(s):  
Fadoua Saadani-Makki ◽  
Sujatha Kannan ◽  
Xin Lu ◽  
James Janisse ◽  
Elizabeth Dawe ◽  
...  
Keyword(s):  
Cerebral Palsy ◽  
Rabbit Model ◽  
Motor Deficits ◽  
Prenatal Infection

scholarly journals Dendrimer-Based Postnatal Therapy for Neuroinflammation and Cerebral Palsy in a Rabbit Model

2012 ◽  
Vol 4 (130) ◽  
pp. 130ra46-130ra46 ◽  
Author(s):  
S. Kannan ◽  
H. Dai ◽  
R. S. Navath ◽  
B. Balakrishnan ◽  
A. Jyoti ◽  
...  
Keyword(s):  
Cerebral Palsy ◽  
Rabbit Model

scholarly journals Hypoxia–ischemia causes persistent movement deficits in a perinatal rabbit model of cerebral palsy: assessed by a new swim test

2009 ◽  
Vol 27 (6) ◽  
pp. 549-557 ◽  
Author(s):  
Matthew Derrick ◽  
Alexander Drobyshevsky ◽  
Xinhai Ji ◽  
Lina Chen ◽  
Yirong Yang ◽  
...  
Keyword(s):  
Cerebral Palsy ◽  
Rabbit Model ◽  
Swim Test ◽  
Hypoxia Ischemia

scholarly journals Enhanced nociception in a rabbit model of cerebral palsy

2021 ◽  
Author(s):  
Emily J Reedich ◽  
Landon T Genry ◽  
Clarissa Fantin Cavarsan ◽  
Elvia Mena Avila ◽  
Meredith A. Singer ◽  
...  
Keyword(s):  
Cerebral Palsy ◽  
Thermal Sensitivity ◽  
Rabbit Model ◽  
Zealand White Rabbit ◽  
Motor Deficits ◽  
Motor Circuits ◽  
Calcitonin Gene ◽  
Isolectin B4 ◽  
The Relationship ◽  
Two Populations

The most prevalent comorbidity of cerebral palsy (CP) is pain. In order to investigate the relationship between perinatal injuries that cause CP and nociception, we investigated mechanical and thermal sensitivity of New Zealand White rabbit kits after prenatal hypoxia-ischemia (HI), sham surgery without hypoxia, and after a typical, unperturbed gestation. A range of motor deficits were observed in kits born naturally after HI (40 minutes at 70-80% gestation) as previously described. We found that HI caused mechanical and thermal allodynia at postnatal day 5, which was accompanied by an expansion of peptidergic afferents (marked by expression of calcitonin gene related peptide; CGRP) in both the superficial and deep dorsal horn. Non-peptidergic afferents (marked by expression of isolectin B4; IB4) were unaltered in HI kits but overlap of the two populations (peptidergic and nonpeptidergic nociceptors) was increased by HI. Interestingly, HI-subjected rabbits exhibited allodynia, even in the absence of motor deficits. HI motor affected and unaffected kits had similar thermal sensitivity but affected kits had less mechanical sensitivity than HI unaffected kits. These findings suggest that prenatal neural injuries impact sensory and motor networks independently and that developing sensory circuits may be more vulnerable than motor circuits to perturbation by prenatal hypoxic-ischemic injury. In conclusion, pain experienced by individuals with CP could arise from developmental insults capable of causing the condition, and therapeutics that specifically target altered nociception in these individuals could be beneficial for treating and preventing chronic pain.

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