期刊
JOURNAL OF PSYCHOPHARMACOLOGY
卷 35, 期 10, 页码 1253-1264出版社
SAGE PUBLICATIONS LTD
DOI: 10.1177/02698811211048281
关键词
Ventral hippocampus; medial prefrontal cortex; venlafaxine; optogenetic stimulation; WKY rat
资金
- NCN [2017/25/B/NZ7/02710]
- Maj Institute of Pharmacology Polish Academy of Sciences
The study investigated the synergistic effects of chronic Venlafaxine and repeated optogenetic stimulation on antidepressant non-responsive rats, and found that the combination was effective in restoring normal behavior. While vHPC-mPFC OGS with VEN treatment supported the hypothesis of antidepressant non-responsiveness, dHPC-mPFC OGS alone was effective in improving behavior in the EPM and NOR tests.
Background: There is extensive evidence that antidepressant drugs restore normal brain function by repairing damage to ventral hippocampus (vHPC) and medial prefrontal cortex (mPFC). While the damage is more extensive in hippocampus, the evidence of treatments, such as deep brain stimulation, suggests that functional changes in prefrontal cortex may be more critical. We hypothesized that antidepressant non-response may result from an insufficiency of transmission from vHPC to mPFC. Method: Antidepressant non-responsive Wistar Kyoto (WKY) rats were subjected to chronic mild stress (CMS), then treated with chronic daily administration of the antidepressant drug venlafaxine (VEN) and/or repeated weekly optogenetic stimulation (OGS) of afferents to mPFC originating from vHPC or dorsal HPC (dHPC). Results: As in many previous studies, CMS decreased sucrose intake, open-arm entries on the elevated plus maze (EPM), and novel object recognition (NOR). Neither VEN nor vHPC-mPFC OGS alone was effective in reversing the effects of CMS, but the combination of chronic VEN and repeated OGS restored normal behaviour on all three measures. dHPC-mPFC OGS restored normal behaviour in the EPM and NOR test irrespective of concomitant VEN treatment, and had no effect on sucrose intake. Conclusions: The synergism between VEN and vHPC-mPFC OGS supports the hypothesis that the antidepressant non-responsiveness of WKY rats results from a failure of antidepressant treatment fully to restore transmission in the vHPC-mPFC pathway.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据