title: The effect of restraint stress on glucocorticoid receptors in mouse spleen lymphocytes: involvement of the sympathetic nervous system.
abstract: OBJECTIVE
  Reciprocal pathways of interaction between the nervous and immune systems during stress may be regulated by stress-induced circulating glucocorticoids that act via type II glucocorticoid receptors (GRs). The aim of the present study was to investigate the effect of restraint stress on GRs in lymphocytes and the role of the sympathetic system in this effect.
  
  
  METHODS
  We used male Balb/c mice which were adrenalectomized 3 days before exposure to restraint stress (4 h). Specific binding of 3H-dexamethasone (Dex) and the expression of GR protein were measured in the cytosol of spleen cells.
  
  
  RESULTS
  Restraint stress caused a significant increase in the maximal binding of 3H-Dex to GRs in the cytosol of spleen cells but not in the binding affinity. In correlation with this increase in binding, restraint stress caused an increase in the amount of GR protein. To establish the relation of the nervous system in this stress response, we blocked the autonomic innervations to the spleen with the ganglionic blocker chlorisondamine. This blocker abrogated the stress-induced increase in the binding of 3H-Dex to GRs and in the GR protein levels. Abrogation of the stress response was also achieved by blocking beta-adrenergic receptors.
  
  
  CONCLUSIONS
  These results suggest that stress-induced increase in the level of GRs is mediated by the sympathetic nervous system via beta-adrenergic receptors. It is possible that stress modulation of lymphocyte GR levels may be implicated in the bidirectional communication between the nervous and the immune systems.
authors.affiliation: Department of Neurology, The Agnes Ginges Center of Human Neurogenetics, Hadassah Hebrew University Hospital, Jerusalem, Israel.
authors.forename: Arielle
authors.initials: A
authors.lastname: Warner
authors.forename: Haim
authors.initials: H
authors.lastname: Ovadia
authors.forename: Nora
authors.initials: N
authors.lastname: Tarcic
authors.forename: Joseph
authors.initials: J
authors.lastname: Weidenfeld
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D016131:Lymphocyte Subsets / Q000166:cytology / Q000378:metabolism*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D015213:Neuroimmunomodulation / Q000276:immunology*; D011965:Receptors, Glucocorticoid / Q000378:metabolism / Q000502:physiology*; D012149:Restraint, Physical; D013154:Spleen / Q000166:cytology / Q000294:innervation / Q000378:metabolism*; D013315:Stress, Psychological / Q000378:metabolism* / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000276:immunology* / Q000378:metabolism
chemical_list: D011965:Receptors, Glucocorticoid