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Serotonin transporter, 5-HT1A receptor, and behavior in DBA/2J mice in comparison with four inbred mouse strains
Nina K Popova1, Vladimir S Naumenko, Marina A Tibeikina
1Department of Behavioral Neurogenomics, Institute of Cytology and Genetics, Siberian Division of Russian Academy of Science, Novosibirsk, Russia.
Abstract:
Prepulse inhibition (PPI), the reduction in acoustic startle produced when it is preceded by a weak prepulse stimulus, is impaired in schizophrenic patients. The DBA/2J mouse strain displayed deficient PPI and is therefore suggested as an experimental animal model for the loss of sensorimotor gating in schizophrenia. Brain serotonin (5-HT) has been implicated in the pathophysiology of several psychiatric disorders, including major depressive disorder and schizophrenia. In the present study, behavior, 5-HT transporter (5-HTT) mRNA level, 5-HT(1A) receptor mRNA level, and 5-HT(1A) receptor density in the brain regions were studied in DBA/2J mice in comparison with four inbred mouse strains (CBA/Lac, C57BL/6, BALB/c, and ICR). A decrease in 5-HTT mRNA level in the midbrain and a reduced density of 5-HT(1A) receptors in the frontal cortex without significant changes in 5-HT(1A) receptor mRNA level in DBA/2J mice were found. It was shown that, along with decreased PPI, DBA/2J mice demonstrated considerably reduced immobility in the tail suspension test and in the forced swim test. No significant interstrain differences in intermale aggression, or in light-dark box and elevated plus-maze tests, were found. The results suggested the involvement of decreased 5-HTT gene expression and 5-HT(1A) receptor density in genetically defined PPI deficiency and showed a lack of any association between PPI deficiency and predisposition to aggressive, anxiety, and depressive-like behaviors.
Insights
DBA/2J mice exhibit impaired prepulse inhibition (PPI), a model for schizophrenia. This deficiency is linked to reduced brain serotonin transporter (5-HTT) gene expression and 5-HT(1A) receptor density, but not anxiety or depression behaviors.
Area of Science:
- Neuroscience
- Psychiatry
- Genetics
Background:
- Prepulse inhibition (PPI) is impaired in schizophrenia patients.
- The DBA/2J mouse strain shows deficient PPI, serving as a potential animal model for schizophrenia's sensorimotor gating deficits.
- Brain serotonin (5-HT) pathways are implicated in psychiatric disorders like schizophrenia.
Purpose of the Study:
- To investigate the neurobiological underpinnings of PPI deficiency in DBA/2J mice.
- To compare DBA/2J mice with other strains regarding behavior and brain serotonin markers.
- To explore the association between PPI deficits and behaviors related to aggression, anxiety, and depression.
Main Methods:
- Behavioral testing including PPI, tail suspension test, forced swim test, aggression assays, light-dark box, and elevated plus-maze.
- Quantification of 5-HT transporter (5-HTT) mRNA levels.
- Measurement of 5-HT(1A) receptor mRNA levels and receptor density in specific brain regions.
Main Results:
- DBA/2J mice displayed significantly reduced PPI.
- A decrease in midbrain 5-HTT mRNA levels and frontal cortex 5-HT(1A) receptor density was observed in DBA/2J mice.
- DBA/2J mice showed reduced immobility in tail suspension and forced swim tests, indicating less depressive-like behavior; no differences in aggression or anxiety-related behaviors were found across strains.
Conclusions:
- Genetically determined PPI deficiency in DBA/2J mice is associated with reduced 5-HTT gene expression and 5-HT(1A) receptor density.
- PPI deficiency in this model is not linked to increased aggressive, anxiety, or depressive-like behaviors.
- These findings contribute to understanding the neurobiology of sensorimotor gating deficits relevant to schizophrenia.
