%0 Journal Article %1 Roberson2006 %A Roberson, Robin %A Woodard, Jade E %A Toso, Laura %A Abebe, Daniel %A Poggi, Sarah H %A Spong, Catherine Y %D 2006 %J Am J Obstet Gynecol %K 2',3'-Cyclic-Nucleotide Phosphodiesterases; Animals; Animals, Newborn; Behavior, Animal; Cerebral Palsy; Disease Models, Female; Humans; Immunohistochemistry; Inflammation; Lipopolysaccharides; Myelin Proteolipid Protein; Pregnancy; Rats; Rats, Inbred F344; Species Specificity %N 4 %P 1038--1044 %R 10.1016/j.ajog.2006.06.046 %T Postnatal inflammatory rat model for cerebral palsy: too different from humans. %U http://dx.doi.org/10.1016/j.ajog.2006.06.046 %V 195 %X OBJECTIVE: In humans, cerebral palsy (CP) may originate from inflammation during the second and third trimesters of gestation when preoligodendrocytes (Pre-OL) are most vulnerable to an inflammatory insult. We studied a postnatal CP model to evaluate injury that would correlate with presence of Pre-OL in human pregnancy. STUDY DESIGN: On postnatal (P) days 2, 3, 4, 5 and 6, pups were treated with (lipopolysaccharide LPS) (n = 7; 30, 30, 60, 60, 120 microg/Kg) or saline (n = 7). Neonates were tested for motor and cognitive development. Adult offspring performed beam walking and rotarod for motor activity. White matter damage was assessed with immunohistochemical Pre-OL markers (CNP, PLP). Statistical analysis included Mann-Whitney U and analysis of variance. RESULTS: LPS-treated animals performed negative geotaxis (P = .009) and surface righting (P = .01) earlier than controls. No differences were observed for other neonatal tests. Adult LPS-treated offspring performed better in tests of motor control: rotarod (P = .01) and beam walking (P = .02). Pre-OL markers were altered in LPS-treated animals at both P22 (CNP and PLP increased in LPS, P < .01 and P < .001, respectively) and 12 weeks (CNP and PLP decreased in LPS, P < .0001 and P < .03, respectively). CONCLUSION: Neonatal exposure to LPS induced white matter damage in the brain, accelerated neurodevelopment and motor tasks in adulthood. These are similar to findings from a postnatal hypoxic model suggesting that in the rodent, targeting the Pre-OL does not result in a CP phenotype.

@article{Roberson2006, abstract = {OBJECTIVE: In humans, cerebral palsy (CP) may originate from inflammation during the second and third trimesters of gestation when preoligodendrocytes (Pre-OL) are most vulnerable to an inflammatory insult. We studied a postnatal CP model to evaluate injury that would correlate with presence of Pre-OL in human pregnancy. STUDY DESIGN: On postnatal (P) days 2, 3, 4, 5 and 6, pups were treated with (lipopolysaccharide [LPS]) (n = 7; 30, 30, 60, 60, 120 microg/Kg) or saline (n = 7). Neonates were tested for motor and cognitive development. Adult offspring performed beam walking and rotarod for motor activity. White matter damage was assessed with immunohistochemical Pre-OL markers (CNP, PLP). Statistical analysis included Mann-Whitney U and analysis of variance. RESULTS: LPS-treated animals performed negative geotaxis (P = .009) and surface righting (P = .01) earlier than controls. No differences were observed for other neonatal tests. Adult LPS-treated offspring performed better in tests of motor control: rotarod (P = .01) and beam walking (P = .02). Pre-OL markers were altered in LPS-treated animals at both P22 (CNP and PLP increased in LPS, P < .01 and P < .001, respectively) and 12 weeks (CNP and PLP decreased in LPS, P < .0001 and P < .03, respectively). CONCLUSION: Neonatal exposure to LPS induced white matter damage in the brain, accelerated neurodevelopment and motor tasks in adulthood. These are similar to findings from a postnatal hypoxic model suggesting that in the rodent, targeting the Pre-OL does not result in a CP phenotype.}, added-at = {2014-07-19T21:08:46.000+0200}, author = {Roberson, Robin and Woodard, Jade E and Toso, Laura and Abebe, Daniel and Poggi, Sarah H and Spong, Catherine Y}, biburl = {https://www.bibsonomy.org/bibtex/2d19ee57df236364da31828755e054ed9/ar0berts}, doi = {10.1016/j.ajog.2006.06.046}, groups = {public}, interhash = {4d0b85dd1e68f5ae4801ead9a6c37760}, intrahash = {d19ee57df236364da31828755e054ed9}, journal = {Am J Obstet Gynecol}, keywords = {2',3'-Cyclic-Nucleotide Phosphodiesterases; Animals; Animals, Newborn; Behavior, Animal; Cerebral Palsy; Disease Models, Female; Humans; Immunohistochemistry; Inflammation; Lipopolysaccharides; Myelin Proteolipid Protein; Pregnancy; Rats; Rats, Inbred F344; Species Specificity}, month = Oct, number = 4, pages = {1038--1044}, pii = {S0002-9378(06)00770-8}, pmid = {17000237}, timestamp = {2014-07-19T21:08:46.000+0200}, title = {Postnatal inflammatory rat model for cerebral palsy: too different from humans.}, url = {http://dx.doi.org/10.1016/j.ajog.2006.06.046}, username = {ar0berts}, volume = 195, year = 2006 }