Substance P alterations in skin and brain of chronically stressed atopic-like mice
2013 (English)In: Journal of the European Academy of Dermatology and Venereology, ISSN 0926-9959, E-ISSN 1468-3083, Vol. 27, no 2, 199-205 p.Article in journal (Refereed) Published
Background Stress is known to worsen the symptoms of atopic eczema (AE). Substance P is likely to play an important role in the development and pathogenesis of AE. less thanbrgreater than less thanbrgreater thanObjective To examine a possible connection between chronic mild stress and changes in the expression of substance P and its receptor (R) neurokinin (NK) 1 in the skin and stress-related brain regions in NC/Nga atopic-like mice. less thanbrgreater than less thanbrgreater thanMethods The mice were divided into three groups (eight animals per group): SE (stressed eczematous), NSE (non-stressed eczematous) and SC (stressed control). Ears and brains of the mice were investigated using immunohistochemistry and RT-PCR. less thanbrgreater than less thanbrgreater thanResults In the skin, there was a decrease in the number of substance P immunoreactive nerve fibres in SE compared with SC group. RT-PCR showed a strong tendency to an increase in mRNA for NK1R in the skin of SE compared with NSE mice. There was an increase in the number of mast cells and the degree of their degranulation in the SE compared with both other groups. less thanbrgreater than less thanbrgreater thanA decrease in substance P immunoreactivity in medial hippocampus was found in SE compared with NSE animals. In prefrontal cortex and central amygdala, there were no significant differences in substance P immunoreactivity between the three groups. less thanbrgreater than less thanbrgreater thanConclusion Exposure to chronic mild stress in NC/Nga atopic-like mice may result in altered expression patterns of substance P in the skin and hippocampus.
Place, publisher, year, edition, pages
Wiley-Blackwell , 2013. Vol. 27, no 2, 199-205 p.
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-89536DOI: 10.1111/j.1468-3083.2011.04443.xISI: 000313883900035OAI: oai:DiVA.org:liu-89536DiVA: diva2:608187
Funding Agencies|Welander/Finsen foundation||Karolinska Institutet||2013-02-262013-02-262013-02-26