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Fear extinction deficits following acute stress associate with increased spine density and dendritic retraction in basolateral amygdala neurons
Authors:Mouna Maroun  Pericles J Ioannides  Krista L Bergman  Alexandra Kavushansky  Andrew Holmes  Cara L Wellman
Institution:1. Sagol Department of Neurobiology, Faculty of Natural Sciences, University of Haifa, , Haifa, Israel;2. Department of Psychological & Brain Sciences and Center for the Integrative Study of Animal Behavior, Indiana University, , Bloomington, IN, USA;3. Indiana University School of Medicine, , Bloomington, IN, USA;4. Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcoholism and Alcohol Abuse, NIH, , Bethesda, MD, USA
Abstract:Stress‐sensitive psychopathologies such as post‐traumatic stress disorder are characterized by deficits in fear extinction and dysfunction of corticolimbic circuits mediating extinction. Chronic stress facilitates fear conditioning, impairs extinction, and produces dendritic proliferation in the basolateral amygdala (BLA), a critical site of plasticity for extinction. Acute stress impairs extinction, alters plasticity in the medial prefrontal cortex‐to‐BLA circuit, and causes dendritic retraction in the medial prefrontal cortex. Here, we examined extinction learning and basolateral amygdala pyramidal neuron morphology in adult male rats following a single elevated platform stress. Acute stress impaired extinction acquisition and memory, and produced dendritic retraction and increased mushroom spine density in basolateral amygdala neurons in the right hemisphere. Unexpectedly, irrespective of stress, rats that underwent fear and extinction testing showed basolateral amygdala dendritic retraction and altered spine density relative to non‐conditioned rats, particularly in the left hemisphere. Thus, extinction deficits produced by acute stress are associated with increased spine density and dendritic retraction in basolateral amygdala pyramidal neurons. Furthermore, the finding that conditioning and extinction as such was sufficient to alter basolateral amygdala morphology and spine density illustrates the sensitivity of basolateral amygdala morphology to behavioral manipulation. These findings may have implications for elucidating the role of the amygdala in the pathophysiology of stress‐related disorders.
Keywords:amygdala  dendritic spine  emotional learning  rat
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