Variant BDNF Val66Met Polymorphism Affects Extinction of Conditioned Aversive Memory

• DOI: 10.1523/jneurosci.5539-08.2009
• Publication Date: 2009-04-01T17:46:04Z
• Authors: Hui Yu; Yue Wang; Siobhan Pattwell; Deqiang Jing; Ting Liu; Yun Zhang; Kevin G. Bath; Francis S. Lee; Zhe-Yu Chen
• Keywords: Extinction (optical mineralogy)

Brain-derived neurotrophic factor (BDNF) plays important roles in activity-dependent plasticity processes, such as long-term potentiation, learning, and memory. The recently reported human BDNF Val66Met (BDNF Met ) polymorphism has been shown to lead altered hippocampal volume impaired hippocampal-dependent memory is associated with a variety of neuropsychiatric disorders. There are few studies, however, that investigate the effect on hippocampal-independent processes. A conditioned taste aversion (CTA) task was used for studying mechanisms long-term, hippocampal-independent, nondeclarative mammalian brain. Using CTA paradigm, we found novel impairment extinction but not acquisition or retention, aversive memories resulting from variant . mice were slower extinguish an compared wild-type counterparts. Moreover, smaller decreased neuronal dendritic complexity ventromedial prefrontal cortex (vmPFC), which significant role CTA. Finally, this delay learning could be rescued pharmacologically cognitive enhancer, d -cycloserine (DCS). To our knowledge, first evidence contributes abnormalities extinction. This abnormality may explained by alterations morphology, well neural activity vmPFC. Importantly, DCS effective rescuing extinction, suggesting when coupled behavior therapy, treatment option anxiety disorders humans genetic BDNF.