Chronic social stress reduces dendritic arbors in CA3 of hippocampus and decreases binding to serotonin transporter sites.
Male rats housed in mixed-sex groups in a visible burrow system (VBS) form a dominance hierarchy in which subordinate animals show stress-related changes in behavior, endocrine function and neurochemistry. Dominants also appear to be moderately stressed compared to controls, although these animals do not develop the more pronounced behavioral and physiological deficits seen in the subordinates. In the present study, we examined the effects of chronic psychosocial stress on the morphology of Golgi-impregnated CA3 pyramidal neurons. In addition, since serotonin has been implicated in the mechanisms mediating the dendritic remodeling seen with other chronic stress regimens, we used quantitative autoradiography to measure binding to the serotonin transporter (5HTT) in hippocampus and dorsal and median raphe. Chronic social stress led to a decrease in the number of branch points and total dendritic length in the apical dendritic trees of CA3 pyramidal neurons in dominant animals compared to unstressed controls; subordinates also had a decreased number of dendritic branch points. [(3)H]paroxetine binding to the 5HTT was decreased in Ammon's horn in both dominants and subordinates compared to controls, while 5HTT binding remained unchanged in dentate gyrus and raphe. The similarity of the changes in 5HTT binding and dendritic arborization between both groups of VBS animals, despite apparent differences in stressor severity, suggests that these changes may be part of the normal adaptive response to chronic social stress. The mechanisms underlying dendritic remodeling in CA3 pyramidal neurons are likely to involve stress-induced changes in glucocorticoids and in 5HT and other transmitters.
McKittrick
C R
CR
Laboratory of Neuroendocrinology, The Rockefeller University, New York, New York 10021, USA. mckittrick@axon.rutgers.edu
Magariños
A M
AM
Blanchard
D C
DC
Blanchard
R J
RJ
McEwen
B S
BS
Sakai
R R
RR
D000818:Animals; D001665:Binding Sites; D001835:Body Weight / Q000502:physiology; D002352:Carrier Proteins / Q000187:drug effects / Q000378:metabolism*; D048429:Cell Size; D002908:Chronic Disease; D003345:Corticosterone / Q000097:blood; D003712:Dendrites / Q000473:pathology / Q000502:physiology; D005260:Female; D006624:Hippocampus / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology*; D008297:Male; D008562:Membrane Glycoproteins / Q000187:drug effects / Q000378:metabolism*; D026901:Membrane Transport Proteins; D009419:Nerve Tissue Proteins; D017374:Paroxetine / Q000494:pharmacology; D017966:Pyramidal Cells / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology*; D011869:Radioligand Assay; D051381:Rats; D020318:Rats, Long-Evans; D050486:Serotonin Plasma Membrane Transport Proteins; D017367:Selective Serotonin Reuptake Inhibitors / Q000494:pharmacology; D013315:Stress, Psychological / Q000503:physiopathology*
D002352:Carrier Proteins; D003345:Corticosterone; D008562:Membrane Glycoproteins; D026901:Membrane Transport Proteins; D009419:Nerve Tissue Proteins; D017374:Paroxetine; D050486:Serotonin Plasma Membrane Transport Proteins; D017367:Selective Serotonin Reuptake Inhibitors; C493232:Slc6a4 protein, rat