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Altered neocortical cell density and layer thickness in serotonin transporter knockout mice: a quantitation study
C Altamura1, M L Dell'Acqua, R Moessner
1Laboratory of Molecular Psychiatry and Neurogenetics, University Campus Bio-Medico, Via Longoni 83, I-00155 Rome, Italy.
Cerebral Cortex (New York, N.Y. : 1991)
|August 15, 2006
Summary
Altering serotonin (5-HT) impacts brain development. Serotonin transporter knockout mice show varied neocortical thickness and cell density, influenced by genetic background, potentially modeling autism development.
Area of Science:
- Neuroscience
- Developmental Biology
- Genetics
Background:
- Serotonin (5-HT) is crucial for development.
- Altered serotonin may link to autism pathogenesis.
- Serotonin transporter (5-HTT) regulates extracellular serotonin levels.
Purpose of the Study:
- To investigate the role of 5-HTT in neocortical development.
- To assess the impact of 5-HTT deficiency on cortical thickness and neuronal density.
- To explore gene-environment interactions in neocortical morphology.
Main Methods:
- Utilized serotonin transporter (5-HTT) knockout (ko) mice.
- Compared neocortical thickness and neuronal cell density with wild-type (wt) mice.
- Analyzed mice with mixed (c129-CD1-C57BL/6J) and pure (C57BL/6J) genetic backgrounds.
Main Results:
- Layer IV thickness decreased in 5-HTT ko mice.
- Cortical thickness changes were dependent on genetic background.
- Increased neuronal cell density observed in 5-HTT ko mice on a C57BL/6J background.
- No significant changes in neuronal density in mixed background ko mice.
Conclusions:
- 5-HTT gene affects neocortical morphology.
- Epistatic interactions with other genes modify 5-HTT's effects.
- Findings may model the influence of 5-HTT variants on neocortical development in autism.
