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Long-term behavioral and acute apopt...

Yuede, Carla M. Timson.

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Long-term behavioral and acute apoptotic neurodegenerative effects of postnatal NMDA-receptor antagonism.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Long-term behavioral and acute apoptotic neurodegenerative effects of postnatal NMDA-receptor antagonism./
Author:	Yuede, Carla M. Timson.
Description:	111 p.
Notes:	Adviser: George Taylor.
Contained By:	Dissertation Abstracts International67-03B.
Subject:	Biology, Neuroscience. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3209941
ISBN:	9780542587481

Long-term behavioral and acute apoptotic neurodegenerative effects of postnatal NMDA-receptor antagonism.
Yuede, Carla M. Timson.

Long-term behavioral and acute apoptotic neurodegenerative effects of postnatal NMDA-receptor antagonism. - 111 p.

Adviser: George Taylor.

Thesis (Ph.D.)--University of Missouri - Saint Louis, 2006.

Administration of an NMDA antagonist to rodents during synaptogenesis can trigger widespread apoptotic neurodegeneration (Ikonomidou et al., 1999). The consequences may be observed later as behavioral dysfunction as a juvenile or an adult. This postnatal developmental period is approximately equal to the last trimester in utero and first several years of human life. Human infants may be exposed to NMDA antagonists in utero by drug-abusing mothers or in the pre and postnatal period through the use of obstetric and pediatric anesthesia. Administering NMDA antagonists at different times within this period induces neuroapoptosis in different brain regions in rodents. The current research was to assess whether this neurodegeneration produces long-term functional deficits. Infant mice were administered different doses of the NMDA antagonist, PCP, at different time points during synaptogenesis in four experiments. Experiment One exposed mice PCP on P7. In Experiment Two mice were exposed to PCP on P2, and Experiment Three exposed mice to PCP on P2 and on P7. In the fourth experiment a separate set of mice was examined for acute apoptotic neurodegeneration with exposure to PCP at each of these time points during development. The general activity, sensorimotor functions, and spatial learning and memory capabilities of the animals were measured during the juvenile period in Experiments One, Two and Three. Pre-pulse inhibition of the startle response, fear conditioning, and spatial learning and memory were also measured in those animals as adults. Behavioral results showed that a single dose of PCP during the postnatal period did not impair long term functioning. However, dosing mice with PCP on P2 and P7 produced significant performance decrements on cognitive tasks without disrupting general activity or gross sensorimotor functioning. Results of Experiment Four indicate significant increases in apoptotic neurodegeneration with a single exposure to PCP at P2 or P7 when compared to saline injection. Exposure at P2+P7 appeared to produce the greatest damage. Results of these studies point to the importance of specific dosing parameters, clarify the long-term effects of postnatal exposure to NMDA antagonists, and identify specific populations of damaged neurons that could be responsible for the functional deficits.

ISBN: 9780542587481Subjects--Topical Terms:

1017680
Biology, Neuroscience.

Long-term behavioral and acute apoptotic neurodegenerative effects of postnatal NMDA-receptor antagonism.
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100 1 $a Yuede, Carla M. Timson. $3 1296414
245 1 0 $a Long-term behavioral and acute apoptotic neurodegenerative effects of postnatal NMDA-receptor antagonism.
300 $a 111 p.
500 $a Adviser: George Taylor.
500 $a Source: Dissertation Abstracts International, Volume: 67-03, Section: B, page: 1745.
502 $a Thesis (Ph.D.)--University of Missouri - Saint Louis, 2006.
520 $a Administration of an NMDA antagonist to rodents during synaptogenesis can trigger widespread apoptotic neurodegeneration (Ikonomidou et al., 1999). The consequences may be observed later as behavioral dysfunction as a juvenile or an adult. This postnatal developmental period is approximately equal to the last trimester in utero and first several years of human life. Human infants may be exposed to NMDA antagonists in utero by drug-abusing mothers or in the pre and postnatal period through the use of obstetric and pediatric anesthesia. Administering NMDA antagonists at different times within this period induces neuroapoptosis in different brain regions in rodents. The current research was to assess whether this neurodegeneration produces long-term functional deficits. Infant mice were administered different doses of the NMDA antagonist, PCP, at different time points during synaptogenesis in four experiments. Experiment One exposed mice PCP on P7. In Experiment Two mice were exposed to PCP on P2, and Experiment Three exposed mice to PCP on P2 and on P7. In the fourth experiment a separate set of mice was examined for acute apoptotic neurodegeneration with exposure to PCP at each of these time points during development. The general activity, sensorimotor functions, and spatial learning and memory capabilities of the animals were measured during the juvenile period in Experiments One, Two and Three. Pre-pulse inhibition of the startle response, fear conditioning, and spatial learning and memory were also measured in those animals as adults. Behavioral results showed that a single dose of PCP during the postnatal period did not impair long term functioning. However, dosing mice with PCP on P2 and P7 produced significant performance decrements on cognitive tasks without disrupting general activity or gross sensorimotor functioning. Results of Experiment Four indicate significant increases in apoptotic neurodegeneration with a single exposure to PCP at P2 or P7 when compared to saline injection. Exposure at P2+P7 appeared to produce the greatest damage. Results of these studies point to the importance of specific dosing parameters, clarify the long-term effects of postnatal exposure to NMDA antagonists, and identify specific populations of damaged neurons that could be responsible for the functional deficits.
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