The University of Texas Medical Branch
Regional and temporal differential regulation of the N-methyl-D-aspartate receptor by phencyclidine during development
Abstract
dc:description.abstractDisruptions in glutamatergic neurotransmission may play a role in the pathogenesis of schizophrenia. The purpose of this study was to determine phencyclidine (PCP)-induced changes in the NMDA receptor subunit composition and the relationship of these changes to the deficits in pre-pulse inhibition (PPI) caused by PCP treatment. Postnatal rats were treated with atypical or typical antipsychotics or selective dopamine or serotonin receptor antagonists prior to acute or sub-chronic PCP. This study provides evidence that two distinct mechanisms underlie effects of acute and sub-chronic PCP on NMDA receptor subunit up-regulation. Furthermore, we discovered that D1, D2, and 5-HT2A receptors play a pivotal role in sub-chronic PCP-induced up-regulation of NR1 and NR2A. Finally, we were able to correlate changes in NMDA receptor subunits to the behavioral effects of PCP in this animal model of schizophrenia.
Degree
thesis:*- Name thesis:degree_name
- Master of Science
- Level thesis:degree_level
- Master
- Grantor
- The University of Texas Medical Branch
- Year dc:date.issued
- 2005
Author and committee
dc:creator, dc:contributor.*- Author dc:creator
-
- Noelle Catherine Anastasio
- Advisor dc:contributor.advisor
-
- Kenneth M. Johnson, PhD.
- Committee members dc:contributor.committeemember
-
- Kathryn Cunningham, PhD.
- Giulio Taglialatela, PhD.
- Geoffrey T. Swanson
Subjects
dc:subject × 3Rights
dc:rights- Statement dc:rights
-
- Copyright © is held by the author. Presentation of this material on the TDL web site by The University of Texas Medical Branch at Galveston was made possible under a limited license grant from the author who has retained all copyrights in the works.
- Language dc:language.iso
- eng
Identifiers
dc:identifier.*- Dc Identifier Other
- etd-07202005-145246
- OAI identifier oai:identifier
- oai:utmb-ir.tdl.org:2152.3/170