title: Chronic restraint stress and chronic corticosterone treatment modulate differentially the expression of molecules related to structural plasticity in the adult rat piriform cortex.
abstract: Stress and stress-related hormones induce structural changes in neurons of the adult CNS. Neurons in the hippocampus, the amygdala and the prefrontal cortex undergo neurite remodeling after chronic stress. In the hippocampus some of these effects can be mimicked with chronic administration of adrenal steroids. These changes in neuronal structure may be mediated by certain molecules related to plastic events such as the polysialylated form of the neural cell adhesion molecule (PSA-NCAM). The expression of PSA-NCAM persists in the adult hippocampus and it is up-regulated after chronic stress. The piriform cortex also displays considerable levels of PSA-NCAM during adulthood and indirect evidence suggests that it may also be the target of stress and stress related-hormones. Using immunohistochemistry we have studied the expression of PSA-NCAM and doublecortin (DCX; another protein implicated in neuronal structural plasticity) in the piriform cortex of adult rats subjected either to 21 days of chronic restraint stress or to oral corticosterone administration during the same period. Our results indicate that chronic stress and chronic corticosterone administration have differential effects on the expression of PSA-NCAM and DCX. While chronic stress increases the number of PSA-NCAM- and DCX-immunoreactive cells in the piriform cortex layer II, chronic corticosterone administration decreases these numbers. These findings indicate that stress and adrenal steroids affect the piriform cortex and suggest that in this region, as in the hippocampus, they may induce structural changes. This is a potential mechanism by which stress and corticosterone modulate functions of this limbic region, such as its participation in olfactory memory.
authors.affiliation: Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10021, USA. nacher@uv.es
authors.forename: J
authors.initials: J
authors.lastname: Nacher
authors.forename: K
authors.initials: K
authors.lastname: Pham
authors.forename: V
authors.initials: V
authors.lastname: Gil-Fernandez
authors.forename: B S
authors.initials: BS
authors.lastname: McEwen
mesh_terms: D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism*; D002908:Chronic Disease; D003345:Corticosterone / Q000008:administration & dosage*; D000089662:Doublecortin Protein; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D008297:Male; D039842:Neural Cell Adhesion Molecule L1 / Q000096:biosynthesis; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012149:Restraint, Physical / Q000379:methods; D012794:Sialic Acids / Q000096:biosynthesis; D013312:Stress, Physiological / Q000188:drug therapy* / Q000378:metabolism*
chemical_list: C000714848:Dcx protein, rat; D000089662:Doublecortin Protein; D039842:Neural Cell Adhesion Molecule L1; D012794:Sialic Acids; C103469:polysialyl neural cell adhesion molecule; D003345:Corticosterone