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Electroencephalographic and early communicative abnormalities in Brattleboro rats
Robert E Lin1, Lauren Ambler, Eddie N Billingslea
1Department of Psychiatry, Translational Neuroscience Program, School of Medicine, University of Pennsylvania Philadelphia, Pennsylvania.
Physiological Reports
|December 5, 2013
Summary
Vasopressin (VP) deficiency in rats impairs vocal communication development and auditory processing in adulthood. This suggests VP system manipulation may treat schizophrenia's negative symptoms.
Area of Science:
- Neuroscience
- Psychiatry
- Genetics
Background:
- Reduced vasopressin (VP) levels and receptors are linked to schizophrenia.
- VP is crucial for social behavior; schizophrenia presents with asociality, potentially developing early.
- Reduced auditory event-related potential (ERP) amplitudes are a schizophrenia endophenotype.
Purpose of the Study:
- To investigate the impact of VP deficiency on vocal communication during development and auditory ERPs in adulthood using Brattleboro (BRAT) rats.
- To explore the age-dependent role of VP in vocalization and auditory processing.
Main Methods:
- Utilized Brattleboro (BRAT) rats, a model of VP deficiency.
- Assessed vocalizations during early postnatal development (days 2, 5, and 9).
- Measured auditory ERPs, including N40 amplitude and gamma intertrial coherence, in adulthood.
Main Results:
- BRAT rats showed normal vocalizations on postnatal days 2 and 5 but exhibited increased vocalization intervals and reduced power from day 9 onwards.
- Adult BRAT rats displayed deficits in auditory ERPs, characterized by reduced N40 amplitude and diminished low and high gamma intertrial coherence.
- These findings indicate age-dependent effects of VP on vocal communication and impaired auditory information processing due to VP reduction.
Conclusions:
- Vasopressin plays a critical, age-dependent role in vocal communication.
- VP deficiency leads to impaired auditory information processing, evidenced by altered ERPs.
- Targeting the vasopressin system may offer a novel therapeutic strategy for negative symptoms in schizophrenia.

