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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Cyclohexanols, Depression, Gene Expression Regulation, Hippocampus, Male, Myocardium, RNA, Messenger, Random Allocation, Rats, Rats, Sprague-Dawley, Stress, Psychological, Venlafaxine Hydrochloride, bcl-2-Associated X Protein, bcl-X Protein.
user
Does venlafaxine modulate depression-induced behaviour and the expression of Bax mRNA and Bcl-xl mRNA in both hippocampus and myocardium? Context: Major depressive disorder is associated with progressive brain changes and is frequently comorbid with cardiovascular disease. There may be shared pathophysiological pathways between cerebral and myocardial dysfunction that impact on apoptosis related proteins. Our aim was to examine behaviour changes of rats with chronic mild stress (CMS), explore the expression of Bax and Bcl-xl in the hippocampus and myocardium, and additionally evaluate the effects of venlafaxine on these molecular mechanisms. Rats were randomly divided into three groups. The behaviour was assessed using the open field and sucrose consumption tests. Gene expression was measured by RT-PCR. In CMS, there was a significant reduction of movements and sucrose consumption, an increased Bax level and a decreased Bcl-xl level in both the hippocampus and myocardium. The venlafaxine group showed an increase in movements and sucrose consumption, as well as upregulated expression of Bcl-xl and downregulated expression of Bax in both the hippocampus and myocardium.
assistant
These results demonstrate that in CMS, there is an increase in pro-apoptotic pathways that is reversed by venlafaxine. This suggests that there are shared active biochemical pathways that may play a role in the process of neuroprogression that is seen in depression and cardiovascular disorders. Final Decision: yes