Archival ReportEffects of Striatal ΔFosB Overexpression and Ketamine on Social Defeat Stress–Induced Anhedonia in Mice
Section snippets
Animals and Drugs
Male C57BL/6J mice (6–8 weeks old) were purchased from Jackson Laboratories (Bar Harbor, Maine), and male CD-1 mice (retired breeders) were purchased from Charles River Laboratories (Wilmington, Massachusetts). Inducible bitransgenic male mice that overexpress ΔFosB were generated from crosses of NSE-tTA (line A) and TetOP-ΔFosB (line A11) mice and fully backcrossed to a C57BL/6J background, using a tetracycline-regulated gene expression system (55). The ΔFosB mice were raised on water
Results
The effects of social defeat on ICSS thresholds were evaluated after each episode of defeat, enabling tracking of changes in responsiveness across the entire CSDS regimen (Figure 1A,B). To facilitate a side-by-side comparison of interval duration effects on ICSS thresholds, LInt and ShInt data are presented together (Figure 1B,C). The effects of CSDS on ICSS thresholds depended on group [F2,22 = 13.53, p < .001] and day [F15,330 = 2.98, p < .001], with a marginal group × day interaction (p =
Discussion
In the ICSS paradigm in mice, CSDS produces anhedonia. Specifically, the present study shows that CSDS decreases the rewarding impact of lateral hypothalamic stimulation, as measured by elevations in ICSS thresholds (19), with effects persisting 5 days following CSDS. These results are broadly consistent with the results of previous studies in rats (59) and hamsters (60), which used other methodologies to quantify brain stimulation reward strength. As expected on the basis of previous work (54)
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