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The Journal of Neuroscience, May 24, 2006, 26(21):5733-5738; doi:10.1523/JNEUROSCI.0474-06.2006
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Brief Communications
Brief Uncontrollable Stress Causes Dendritic Retraction in Infralimbic Cortex and Resistance to Fear Extinction in Mice
Alicia Izquierdo,1 * Cara L. Wellman,2 * andAndrew Holmes1 1Section on Behavioral Science and Genetics, Laboratory for Integrative Neuroscience, National Institute on Alcoholism and Alcohol Abuse, National Institutes of Health, Rockville, Maryland 20852, and 2Department of Psychological and Brain Sciences and Program in Neuroscience, Indiana University, Bloomington, Indiana 47405
Correspondence should be addressed to Dr. Alicia Izquierdo, California State University, Los Angeles, College of Natural and Social Sciences, Department of Psychology, 5151 State University Drive, Los Angeles, CA 90032. Email: AIzquie{at}calstatela.edu
Extinction of conditioned fear responses is an active learning process resulting from the repeated presentation of a conditioned stimulus in the absence of the unconditioned aversive stimulus. Recent research implicates the medial prefrontal cortex (mPFC) in the mediation of fear extinction in rodents and the pathophysiology of posttraumatic stress disorder. However, there is currently little understanding of precisely how stress can impact fear extinction and the neural circuitry subserving this behavior. The present study examined the effects of brief exposure to an uncontrollable stressor on (1) fear conditioning and fear extinction, and (2) dendritic morphology of pyramidal neurons in the infralimbic (IL) and prelimbic (PL) regions of the mPFC in mice. Exposure to three episodes of stress ending 24 h before fear conditioning significantly attenuated the rate of cued fear extinction relative to nonstressed controls, but did not affect fear conditioning or cue or context recall. Analysis of Golgi-stained neurons showed that one or three exposures to daily swim stress caused significant retraction of terminal branches of apical, but not basilar, dendrites of IL neurons. In contrast, PL neuronal morphology was unaltered by stress. These data demonstrate that IL, but not PL, neurons are highly sensitive to even brief exposure to stress, and that this same form of stress impairs fear extinction. Present findings suggest that trauma may compromise the functional integrity of the mPFC with implications for the pathophysiology of certain neuropsychiatric disorders.
Key words: stress; infralimbic cortex; fear extinction; mPFC; PTSD; dendritic arborization
Received Sept. 9, 2005; revised March 30, 2006; accepted April 1, 2006.
Correspondence should be addressed to Dr. Alicia Izquierdo, California State University, Los Angeles, College of Natural and Social Sciences, Department of Psychology, 5151 State University Drive, Los Angeles, CA 90032. Email: AIzquie{at}calstatela.edu
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