Central nervous system activation following peripheral chemical sympathectomy: Implications for neural-immune interactions

被引:13
|
作者
Callahan, TA [1 ]
Moynihan, JA
Piekut, DT
机构
[1] Univ Rochester, Sch Med & Dent, Grad Program Neurosci, Rochester, NY 14642 USA
[2] Univ Rochester, Sch Med & Dent, Ctr Psychoneuroimmunol Res, Rochester, NY 14642 USA
[3] Univ Rochester, Sch Med & Dent, Dept Neurobiol & Anat, Rochester, NY 14642 USA
[4] Univ Rochester, Sch Med & Dent, Dept Psychiat, Rochester, NY 14642 USA
[5] Univ Rochester, Sch Med & Dent, Dept Microbiol & Immunol, Rochester, NY 14642 USA
关键词
hypothalamic-pituitary-adrenal (HPA) axis; sympathetic nervous system (SNS); corticotrophin-releasing factor (CRF); tyrosine hydroxylase (TH); arginine-vasopressin (AVP); adrenocorticotrophin (ACTH);
D O I
10.1006/brbi.1998.0526
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Many studies have demonstrated that ablation of the sympathetic nervous system (SNS) alters subsequent immune responses. Researchers have presumed that the altered immune responses are predominantly the result of the peripheral phenomenon of denervation. We, however, hypothesized that chemical sympathectomy will signal and activate the central nervous system (CNS). Activation of the CNS was determined by immunocytochemical visualization of Fos protein in brains from male C57BL/6 mice at 8, 24, and 48 h following denervation. A dramatic induction of Fos protein was found in the paraventricular nucleus (PVN) of the hypothalamus and other specific brain regions at 8 and 24 h compared to vehicle control mice. Dual-antigen labeling demonstrates that corticotrophin releasing factor (CRF)-containing neurons in the PVN are activated by chemical sympathectomy; however, neurons containing neurotransmitters which may modulate CRF neurons, such as vasopressin, tyrosine hydroxylase, and adrenocorticotropin, do not coexpress Fos. Our findings suggest an involvement of the CNS in sympathectomy-induced alterations of immunity. (C) 1998 Academic Press.
引用
收藏
页码:230 / 241
页数:12
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