CNFA 2005 SfN Abstracts
 
CHRONIC STRESS INDUCES DENDRITIC ALTERATIONS IN PYRAMIDAL CELLS OF THE INFRALIMBIC CORTEX
D.S.Goldwater1,2*; C.Liston3; M.M.Miller3; B.S.McEwen3; J.H.Morrison1,2
1. Fishberg Department of Neuroscience, 2. Kastor Neurobiology of Aging Laboratories, Mount Sinai School of Medicine, New York City, NY, USA
3. Rockefeller Univ., New York, NY, USA
Chronic stress has been shown to cause dendritic retraction of pyramidal cells in the hippocampus (Watanabe et al., 1992). More recently, loss of dendritic arbor in pyramidal cells within the anterior cingulate cortex was demonstrated (Radley et al., 2004). In contrast, chronic stress augments dendritic arbor in the lateral amygdala (Vyas et al, 2002). Such morphologic adjustments could alter the connectivity and balance of activity between these three regions, providing a substrate for the long-term behavioral consequences of stress. We have now extended this approach to the infralimbic cortex, a region known to modulate the amygdala in the context of fear responses (Milad and Quirk, 2002). We are investigating the effects of both chronic stress and potential for reversibility of such effects on pyramidal cell morphology in the infralimbic area of the prefrontal cortex. Rats were subjected to 6 hours of daily restraint stress for 21 consecutive days. The animals were then perfused either immediately after the 21 days of stress or three weeks following the final day of restraint stress. The infralimbic area was sectioned at 250m and pyramidal neurons in layer II/III were injected with Lucifer Yellow. 3-Dimensional reconstructions of the injected neurons were carried out using Neurolucida in order to determine the effects of chronic stress on total dendritic length, branch number, and dendritic complexity, as well as the potential for these effects to be reversed by an extended recovery period. Preliminary results from Sholl analysis suggest chronic stress induces a retraction of the most distal branches of the apical dendritic tree, particularly between 270m and 360m from the cell body. Additional analyses relevant both to chronic stress as well as the potential reversibility of these effects are underway.
Support Contributed By: NIH grant MH58911