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Effects of chronic mild stress in female bax inhibitor-1-gene knockout mice.

Sui ZY, Chae HJ, Huang GB, Zhao T, Shrestha Muna S, Chung YC - Clin Psychopharmacol Neurosci (2012)

Bottom Line: Significant decreases in sucrose consumption and increases in immobility time in the FST were observed in both stress groups compared with the non-stress groups.These results suggest that BI-1 may play role in protecting against the depressogenic effects of CMS in the short term, but not in the long term.Further study is required to deepen understanding of the role of BI-1 in protecting against depression.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychiatry, Chonbuk National University Medical School & Institute for Medical Sciences, Jeonju, Korea. ; Department of Psychiatry, Chonbuk National University Hospital & Research Institute of Clinical Medicine, Jeonju, Korea.

ABSTRACT

Objective: The anti-apoptotic protein Bax inhibitor-1 (BI-1) is a regulator of apoptosis linked to endoplasmic reticulum (ER) stress, and BI-1(-/-) mice exhibit increased sensitivity to tissue damage. The purpose of this study was to investigate the role of BI-1 in the pathogenesis of chronic mild stress (CMS)-induced depression-like behaviors in BI-1(-/-) mice.

Methods: We delivered CMS for 2 or 6 weeks in BI-1-knockout and wild-type mice. Control groups of BI-1-knockout and wild-type mice were left undisturbed. The measured parameters were sucrose consumption at weeks 1, 2, 3, 4, 5, and 6, spontaneous locomotion, and a forced swimming test (FST) at weeks 2 and 6.

Results: Significant decreases in sucrose consumption and increases in immobility time in the FST were observed in both stress groups compared with the non-stress groups. Interestingly, at week 2, but not at week 6, BI-1(-/-)-stress mice showed less sucrose intake and greater immobility time than did BI-1(+/+)-stress mice.

Conclusion: These results suggest that BI-1 may play role in protecting against the depressogenic effects of CMS in the short term, but not in the long term. Further study is required to deepen understanding of the role of BI-1 in protecting against depression.

No MeSH data available.


Related in: MedlinePlus

(A) Effect of chronic mild stress on sucrose consumption over 6 weeks and (B) effect of chronic mild stress in sucrose consumption at week 2. *Significant differences from BI-1-/--control (*p<0.05, **p<0.01, ***p<0.001); †significant difference from BI-1+/+-control (††p<0.01, †††p<0.001); ‡significant difference from BI-1-/--stress (‡‡p<0.01, ‡‡‡p<0.001). BI-1, Bax inhibitor-1.
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Figure 3: (A) Effect of chronic mild stress on sucrose consumption over 6 weeks and (B) effect of chronic mild stress in sucrose consumption at week 2. *Significant differences from BI-1-/--control (*p<0.05, **p<0.01, ***p<0.001); †significant difference from BI-1+/+-control (††p<0.01, †††p<0.001); ‡significant difference from BI-1-/--stress (‡‡p<0.01, ‡‡‡p<0.001). BI-1, Bax inhibitor-1.

Mentions: The ANOVA yielded a significant main effect of group (F[3,17]=92.562, p<0.001) and time (F[6,102]=44.123, p<0.001) and a significant group×time interaction (F[18,102]=4.460, p<0.001) for sucrose consumption (Fig. 3A, 3B). A post hoc group analysis demonstrated significant differences between the BI-1+/+-control group vs. the BI-1+/+-stress group and between the BI-1-/--stress and BI-1+/+-stress groups vs. the BI-1-/--control group as well as between the BI-1-/--stress and the BI-1-/--stress groups vs. the BI-1-/--control group. The BI-1+/+-stress and BI-1-/--stress groups consumed significantly less sucrose than the BI-1+/+-control and BI-1-/--control groups, starting from week 1 and throughout the experiment. No significant differences in sucrose consumption were observed between BI-1+/+-control BI-1-/--control groups throughout the experiment, except at week 1, when greater sucrose was consumed in the BI-1-/--control group than in the BI-1+/+-control group (F=20.733, p=0.018). Interestingly, at week 2, less sucrose was consumed in the BI-1-/--stress group than in the BI-1+/+-stress group (F=28.592, p<0.001) (Fig. 3B).


Effects of chronic mild stress in female bax inhibitor-1-gene knockout mice.

Sui ZY, Chae HJ, Huang GB, Zhao T, Shrestha Muna S, Chung YC - Clin Psychopharmacol Neurosci (2012)

(A) Effect of chronic mild stress on sucrose consumption over 6 weeks and (B) effect of chronic mild stress in sucrose consumption at week 2. *Significant differences from BI-1-/--control (*p<0.05, **p<0.01, ***p<0.001); †significant difference from BI-1+/+-control (††p<0.01, †††p<0.001); ‡significant difference from BI-1-/--stress (‡‡p<0.01, ‡‡‡p<0.001). BI-1, Bax inhibitor-1.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3569165&req=5

Figure 3: (A) Effect of chronic mild stress on sucrose consumption over 6 weeks and (B) effect of chronic mild stress in sucrose consumption at week 2. *Significant differences from BI-1-/--control (*p<0.05, **p<0.01, ***p<0.001); †significant difference from BI-1+/+-control (††p<0.01, †††p<0.001); ‡significant difference from BI-1-/--stress (‡‡p<0.01, ‡‡‡p<0.001). BI-1, Bax inhibitor-1.
Mentions: The ANOVA yielded a significant main effect of group (F[3,17]=92.562, p<0.001) and time (F[6,102]=44.123, p<0.001) and a significant group×time interaction (F[18,102]=4.460, p<0.001) for sucrose consumption (Fig. 3A, 3B). A post hoc group analysis demonstrated significant differences between the BI-1+/+-control group vs. the BI-1+/+-stress group and between the BI-1-/--stress and BI-1+/+-stress groups vs. the BI-1-/--control group as well as between the BI-1-/--stress and the BI-1-/--stress groups vs. the BI-1-/--control group. The BI-1+/+-stress and BI-1-/--stress groups consumed significantly less sucrose than the BI-1+/+-control and BI-1-/--control groups, starting from week 1 and throughout the experiment. No significant differences in sucrose consumption were observed between BI-1+/+-control BI-1-/--control groups throughout the experiment, except at week 1, when greater sucrose was consumed in the BI-1-/--control group than in the BI-1+/+-control group (F=20.733, p=0.018). Interestingly, at week 2, less sucrose was consumed in the BI-1-/--stress group than in the BI-1+/+-stress group (F=28.592, p<0.001) (Fig. 3B).

Bottom Line: Significant decreases in sucrose consumption and increases in immobility time in the FST were observed in both stress groups compared with the non-stress groups.These results suggest that BI-1 may play role in protecting against the depressogenic effects of CMS in the short term, but not in the long term.Further study is required to deepen understanding of the role of BI-1 in protecting against depression.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychiatry, Chonbuk National University Medical School & Institute for Medical Sciences, Jeonju, Korea. ; Department of Psychiatry, Chonbuk National University Hospital & Research Institute of Clinical Medicine, Jeonju, Korea.

ABSTRACT

Objective: The anti-apoptotic protein Bax inhibitor-1 (BI-1) is a regulator of apoptosis linked to endoplasmic reticulum (ER) stress, and BI-1(-/-) mice exhibit increased sensitivity to tissue damage. The purpose of this study was to investigate the role of BI-1 in the pathogenesis of chronic mild stress (CMS)-induced depression-like behaviors in BI-1(-/-) mice.

Methods: We delivered CMS for 2 or 6 weeks in BI-1-knockout and wild-type mice. Control groups of BI-1-knockout and wild-type mice were left undisturbed. The measured parameters were sucrose consumption at weeks 1, 2, 3, 4, 5, and 6, spontaneous locomotion, and a forced swimming test (FST) at weeks 2 and 6.

Results: Significant decreases in sucrose consumption and increases in immobility time in the FST were observed in both stress groups compared with the non-stress groups. Interestingly, at week 2, but not at week 6, BI-1(-/-)-stress mice showed less sucrose intake and greater immobility time than did BI-1(+/+)-stress mice.

Conclusion: These results suggest that BI-1 may play role in protecting against the depressogenic effects of CMS in the short term, but not in the long term. Further study is required to deepen understanding of the role of BI-1 in protecting against depression.

No MeSH data available.


Related in: MedlinePlus