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Published on: August 24, 2012
Variant BDNF Val66Met polymorphism affects extinction of conditioned aversive memory
Hui Yu1, Yue Wang, Siobhan Pattwell
1Department of Neurobiology, School of Medicine, Shandong University, Jinan, Shandong 250012, China.
Summary
The BDNF Val66Met polymorphism impairs memory extinction, a type of hippocampal-independent learning. This delay in extinction learning was reversed by d-cycloserine, suggesting a potential treatment for related anxiety disorders.
Area of Science:
- Neuroscience
- Genetics
- Behavioral Science
Background:
- Brain-derived neurotrophic factor (BDNF) is crucial for learning and memory.
- The BDNF Val66Met polymorphism is linked to hippocampal changes and memory deficits.
- Limited research exists on BDNF Val66Met's impact on hippocampal-independent memory.
Purpose of the Study:
- To investigate the effect of the BDNF Val66Met polymorphism on hippocampal-independent memory extinction.
- To explore the role of the ventromedial prefrontal cortex (vmPFC) in BDNF Val66Met-associated memory deficits.
- To assess the potential of d-cycloserine (DCS) in rescuing impaired extinction learning.
Main Methods:
- Utilized a conditioned taste aversion (CTA) paradigm in mice to model hippocampal-independent memory.
- Compared extinction learning, acquisition, and retention between BDNF Val66Met variant mice and wild-type counterparts.
- Examined vmPFC volume and neuronal dendritic complexity, and tested DCS administration for rescuing extinction deficits.
Main Results:
- BDNF Val66Met mice exhibited impaired extinction learning of aversive memories, but not acquisition or retention.
- A smaller vmPFC volume and reduced neuronal dendritic complexity were associated with the BDNF(Met) polymorphism.
- D-cycloserine (DCS) successfully rescued the delay in extinction learning in BDNF Val66Met mice.
Conclusions:
- The BDNF Val66Met polymorphism specifically impairs memory extinction, a hippocampal-independent process.
- Alterations in vmPFC morphology and neural activity likely underlie the observed extinction deficits.
- DCS shows promise as a therapeutic agent for memory extinction impairments in individuals with the BDNF Val66Met variant, potentially aiding in anxiety disorder treatment.
