BLUNTED SENSITIVITY TO SUCROSE IN AUTOIMMUNE MRL-IPR MICE - A CURVE-SHIFT STUDY

Citation
B. Sakic et al., BLUNTED SENSITIVITY TO SUCROSE IN AUTOIMMUNE MRL-IPR MICE - A CURVE-SHIFT STUDY, Brain research bulletin, 41(5), 1996, pp. 305-311
Citations number
53
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
03619230
Volume
41
Issue
5
Year of publication
1996
Pages
305 - 311
Database
ISI
SICI code
0361-9230(1996)41:5<305:BSTSIA>2.0.ZU;2-5
Abstract
Lupus-prone MRL-lpr mice show an autoimmunity-associated behavioral sy ndrome that has many features similar to the effects of chronic stress . The present study evaluated whether autoimmune MRL-lpr mice show red uced responsiveness to sucrose, as observed in normal animals exposed to chronic mild stress. Sixteen-week old MRL-lpr mice and their age-ma tched congenic MRL +/+ controls were given 0%, 0.5% 1%, 2%, 4%, 8%, or 16% sucrose solution to drink every 48 h in a one-bottle test. The MR L-lpr mice drank less than controls at all concentrations, except at 1 6%, The amount of sucrose consumed vs. solution concentration followed a saturation curve. Estimates were obtained for the concentration yie lding the half-maximum response (X(50)) and the response at saturating concentration of sucrose (R(max)). The X(50) was significantly higher in MRL-lpr than in MRL +/+ mice, indicating a shift to the right of t he concentration-intake curve. The R(max) did not differ significantly between substrains, suggesting that the autoimmune process did not af fect performance capacity. Pretreatment with the immunosuppressant cyc lophosphamide diminished the substrain difference in X(50), suggesting that reduced sensitivity to sucrose is related to autoimmune/inflamma tory factors. These results support the similarity between autoimmunit y-associated behavioral syndrome and behavioral changes produced by ch ronic stress, and suggest common neuroendocrine mechanisms. Because re duced sensitivity to palatable stimulus may reflect blunted hedonic re sponsiveness (''anhedonia''), it is hypothesized that an autoimmune/in flammatory factor(s) produces the depression found in human lupus, and some cases of affective disorder. Copyright (C) 1996 Elsevier Science Inc.