Effects of acute and repeated administration of Staphylococcal enterotoxin A on Morris water maze learning, corticosterone and hippocampal IL-1β and TNFα

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• 作者：Randall T. Woodruff^a ; Kristen M. Schorpp^a ; Agniesczka J. Lawrenczyk^a ; Trisha Chakraborty^a ; Alexander W. Kusnecov^a ; ^b ; ^{kusnecov@rci.rutgers.edu"" rel=""nofollow}
• 关键词：Staphylococcal enterotoxin A ; Cytokines ; Corticosterone ; Interleukin-1β ; Tumor necrosis factor ; Interleukin-2 ; Morris water maze ; Learning ; Hippocampus ; T cells
• 刊名：Brain, Behavior, and Immunity
• 出版年：2011
• 出版时间：July 2011
• 年：2011
• 卷：25
• 期：5
• 页码：938-946
• 全文大小：549 K

文摘

Staphylococcal enterotoxin A (SEA) is a bacterial superantigen that induces pronounced T cell expansion and cytokine production. In addition, SEA activates the HPA axis and forebrain regions relevant to cognitive functions. Since learning-related cognitive changes have not been assessed in response to SEA, spatial learning in the Morris water maze (MWM) was determined in male C57BL/6 J mice subjected to acute or repeated injections of 5 μg SEA or Saline. Injections were given 2 h prior to 4–5 days of hidden platform sessions. Animals were then rested for 1 month and given retraining without further injections. In addition, splenic IL-1β, IL-2 and TNFα, plasma corticosterone, and hippocampal IL-1β and TNFα were measured after the regimen of treatment used in the behavioral experiments. The results showed no learning impairment following acute or repeated SEA challenge. Moreover, when retested 1 month later, and without further injections, the SEA group showed more rapid relearning of the MWM. This suggested that coincidental superantigenic T cell activation and training served to promote long-term improvement in recovery of learning. Furthermore, repeated SEA challenge continued to drive increases in plasma corticosterone, but with a compensatory reduction in hippocampal IL-1β. However, while hippocampal TNFα was reduced after acute and repeated SEA treatment, this was not statistically significant. In view of the importance of modest glucocorticoid elevations and hippocampal IL-1β in promoting contextual learning, the data point to the hypothesis that SEA promotes long-term plasticity by restraining disruptive increases in hippocampal IL-1β, and possibly TNFα, during learning.