Preethi Hegde1, Shane O'Mara2, Thenkanidiyoor Rao Laxmi1. 1. Department of Neurophysiology, National Institute of Mental Health and Neurosciences, Bangalore, India. 2. School of Psychology and Trinity College Institute of Neuroscience, Trinity College, Dublin, Ireland.
Abstract
BACKGROUND: Extinction of fear memory depends on the environmental and emotional cues. Furthermore, consolidation of extinction is also dependent on the environmental exposure. But, the relationship of the time of the exposure to a variety of environmental cues is not well known. The important region involved in facilitation of extinction of fear memory is through diversion of the flow of information leaving the lateral nucleus of amygdala. PURPOSE: The study aimed to address a question to explain how these brain regions react to environmental stimulation during the retention and extinction of fear memory. METHODS: An enriched environment (EE) is assumed to mediate extinction of fear memory, we examined the apparent discrepancy between the effects of defensive response, the freezing behavior induced by Pavlovian classical fear conditioning by subjecting them to variance in the timing to EE. The different timing of EE exposure was 10 days of EE either before fear conditioning and/or after extinction training to the rats. The local field potentials was recorded from CA1 hippocampus, lateral nucleus of amygdala and infralimbic region of medial prefrontal cortex (mPFC) during the fear learning and extinction from the control rats and rats exposed to EE before and after fear conditioning. RESULTS: Exposure to EE before the fear conditioning and after extinction training was more effective in the extinction fear memory. In addition, we also found switching from exploratory locomotion to freezing during retention of contextual fear memory which was associated with decreased theta power and reduced synchronized theta oscillations in CA1-hippocampus, lateral nucleus of amygdala, and infralimbic region of mPFC. CONCLUSION: Thus, we propose that the timing of exposure to EE play a key role in the extinction of fear memory.
BACKGROUND: Extinction of fear memory depends on the environmental and emotional cues. Furthermore, consolidation of extinction is also dependent on the environmental exposure. But, the relationship of the time of the exposure to a variety of environmental cues is not well known. The important region involved in facilitation of extinction of fear memory is through diversion of the flow of information leaving the lateral nucleus of amygdala. PURPOSE: The study aimed to address a question to explain how these brain regions react to environmental stimulation during the retention and extinction of fear memory. METHODS: An enriched environment (EE) is assumed to mediate extinction of fear memory, we examined the apparent discrepancy between the effects of defensive response, the freezing behavior induced by Pavlovian classical fear conditioning by subjecting them to variance in the timing to EE. The different timing of EE exposure was 10 days of EE either before fear conditioning and/or after extinction training to the rats. The local field potentials was recorded from CA1 hippocampus, lateral nucleus of amygdala and infralimbic region of medial prefrontal cortex (mPFC) during the fear learning and extinction from the control rats and rats exposed to EE before and after fear conditioning. RESULTS: Exposure to EE before the fear conditioning and after extinction training was more effective in the extinction fear memory. In addition, we also found switching from exploratory locomotion to freezing during retention of contextual fear memory which was associated with decreased theta power and reduced synchronized theta oscillations in CA1-hippocampus, lateral nucleus of amygdala, and infralimbic region of mPFC. CONCLUSION: Thus, we propose that the timing of exposure to EE play a key role in the extinction of fear memory.
Entities:
Keywords:
Context; Differential fear conditioning; Enriched environment; Extinction; Freezing
Authors: G C W Wendel-Vos; A J Schuit; E J M Feskens; H C Boshuizen; W M M Verschuren; W H M Saris; D Kromhout Journal: Int J Epidemiol Date: 2004-05-27 Impact factor: 7.196