Neuroscience 2005 Abstract
| Presentation Number: | 1021.8 |
|---|---|
| Abstract Title: | Dissociation of neuroanatomical abnormalities from cognitive deficits associated with schizophrenia in transgenic mice overexpressing Gαs. |
| Authors: |
Esposito, M. F.*1
; Kelly, M. P.1,2
; Siegel, S. J.2
; Kanes, S. J.2
; Abel, T.1
1Biology, Univ. of Pennsylvania, Philadelphia, PA 2Psychiatry, Univ. of Pennsylvania, Philadelphia, PA |
| Primary Theme and Topics |
Disorders of the Nervous System - Cognitive, Emotional and Behavioral State Disorders -- Schizophrenia: Animal models |
| Secondary Theme and Topics | Cognition and Behavior<br />- Animal Cognition and Behavior<br />-- Cognitive learning and memory systems |
| Session: |
1021. Schizophrenia: Genetic Models Poster |
| Presentation Time: | Wednesday, November 16, 2005 4:00 PM-5:00 PM |
| Location: | Washington Convention Center - Hall A-C, Board # UU10 |
| Keywords: | G-protein, Mouse Model, Neuroanatomy, Ventricle |
Patients with schizophrenia exhibit alterations in neuroanatomy, particularly an enlargement of the lateral ventricles, but it remains unclear if these structural changes cause the behavioral deficits associated with the disease or if they are simply secondary to an initial biochemical insult (Shenton ME et al., 2001, Schizophrenia Research, 49, 32-33). We have developed a line of transgenic mice overexpressing a wildtype isoform of the G-protein subunit Gαs (Gαswt) that exhibits a number of cognitive deficits associated with schizophrenia (see Kelly MP et al., 2005, SFN abstract). Here we explore if these cognitive deficits are due to neuroanatomical abnormalities such as those observed in schizophrenia patients. In sagittal sections (Lateral 0.84-1.32mm), Gαswt transgenic mice exhibit enlarged lateral ventricles, reduced caudate putamen, and reduced nucleus accumbens with no change in total brain size. Although acute suppression of the transgene during adulthood by doxycycline rescues the observed cognitive deficits in Gαswt transgenic mice, it does not reverse the noted anatomical abnormalities. This reveals a dissociation of anatomical abnormalities from behavior, suggesting that structural changes are secondary to the overexpression of Gαswt, and that the structural changes themselves do not cause the noted behavioral symptoms. This result proves promising in the development of therapeutics for the treatment of schizophrenia because behavioral deficits can be rescued independent of altering neuroanatomy.
Supported by NIH; Merck, Whitehall, and Packard Foundations, as well as the Tourette’s Syndrome Association
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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