Related Experiment Video
Updated: Jun 3, 2026
Assessing Social Dominance in Mouse Models Using the Tube Test
Published on: June 6, 2025
Cognitive and socio-emotional deficits in platelet-derived growth factor receptor-β gene knockout mice
Phuong Thi Hong Nguyen1, Tomoya Nakamura, Etsuro Hori
1System Emotional Science, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
Insights
Mice lacking Platelet-Derived Growth Factor Receptor Beta (PDGFR-β) in neurons exhibit significant deficits in cognitive and social behaviors. This suggests PDGFR-β is crucial for normal brain function and may contribute to conditions like autism and schizophrenia.
Area of Science:
- Neuroscience
- Developmental Biology
- Genetics
Background:
- Platelet-Derived Growth Factor (PDGF) is a key mitogen involved in embryogenesis and central nervous system (CNS) development.
- PDGF and its receptor, PDGFR-β, are implicated in schizophrenia and autism spectrum disorders.
- The behavioral impact of PDGFR-β deletion in CNS neurons has not been previously studied.
Purpose of the Study:
- To investigate the behavioral and neurophysiological consequences of conditional PDGFR-β deletion in CNS neurons of mice.
- To explore the potential role of PDGFR-β in cognitive and socioemotional functions.
Main Methods:
- Generation of novel PDGFR-β knockout (KO) mice using the Cre/loxP system for conditional deletion in CNS neurons.
- Comprehensive behavioral testing including spatial memory, social interaction, conditioning, prepulse inhibition, and forced swimming.
- Immunohistochemical analysis of parvalbumin-positive neurons and neurophysiological assessment of gamma oscillations.
Main Results:
- PDGFR-β KO mice showed no apparent anatomical defects but exhibited deficits across all tested behavioral domains.
- A reduction in parvalbumin-positive neurons was observed in key brain regions (amygdala, hippocampus, medial prefrontal cortex).
- Sensory-evoked gamma oscillations were diminished in PDGFR-β KO mice, correlating with reduced parvalbumin neuron counts.
Conclusions:
- Conditional deletion of PDGFR-β in CNS neurons impairs cognitive and socioemotional behaviors in mice.
- PDGFR-β is essential for normal functioning of parvalbumin-ergic neurons and gamma oscillations.
- These findings suggest that PDGFR-β deficits may contribute to the pathophysiology of schizophrenia and autism.
Abstract:
Platelet-derived growth factor (PDGF) is a potent mitogen. Extensive in vivo studies of PDGF and its receptor (PDGFR) genes have reported that PDGF plays an important role in embryogenesis and development of the central nervous system (CNS). Furthermore, PDGF and the β subunit of the PDGF receptor (PDGFR-β) have been reported to be associated with schizophrenia and autism. However, no study has reported on the effects of PDGF deletion on mice behavior. Here we generated novel mutant mice (PDGFR-β KO) in which PDGFR-β was conditionally deleted in CNS neurons using the Cre/loxP system. Mice without the Cre transgene but with floxed PDGFR-β were used as controls. Both groups of mice reached adulthood without any apparent anatomical defects. These mice were further examined by conducting several behavioral tests for spatial memory, social interaction, conditioning, prepulse inhibition, and forced swimming. The test results indicated that the PDGFR-β KO mice show deficits in all of these areas. Furthermore, an immunohistochemical study of the PDGFR-β KO mice brain indicated that the number of parvalbumin (calcium-binding protein)-positive (i.e., putatively γ-aminobutyric acid-ergic) neurons was low in the amygdala, hippocampus, and medial prefrontal cortex. Neurophysiological studies indicated that sensory-evoked gamma oscillation was low in the PDGFR-β KO mice, consistent with the observed reduction in the number of parvalbumin-positive neurons. These results suggest that PDGFR-β plays an important role in cognitive and socioemotional functions, and that deficits in this receptor may partly underlie the cognitive and socioemotional deficits observed in schizophrenic and autistic patients.
