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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Erburu, M. Cajaleon, L. Guruceaga, E. Venzala, E. Muñoz-Cobo, I. Beltrán, E. Puerta, E. Tordera, R. M. |
| Description | Country affiliation: Spain Author Affiliation: Erburu M ( Department of Pharmacology, University of Navarra, 31008 Pamplona, Spain.); Cajaleon L ( Department of Pharmacology, University of Navarra, 31008 Pamplona, Spain.); Guruceaga E ( Bioinformatics Unit, Center for Applied Medical Research, University of Navarra, 31008 Pamplona, Spain); Venzala E ( Department of Pharmacology, University of Navarra, 31008 Pamplona, Spain.); Muñoz-Cobo I ( Department of Pharmacology, University of Navarra, 31008 Pamplona, Spain.); Beltrán E ( Department of Pharmacology, University of Navarra, 31008 Pamplona, Spain.); Puerta E ( Department of Pharmacology, University of Navarra, 31008 Pamplona, Spain); Tordera RM ( Department of Pharmacology, University of Navarra, 31008 Pamplona, Spain) |
| Abstract | Many studies suggest that the prefrontal cortex (PFC) is a target limbic region for stress response because a dysfunction here is linked to anhedonia, a decrease in reactivity to rewards, and to anxiety. It is suggested that stress-induced persistent molecular changes in this brain region could bring some light on the mechanisms perpetuating depressive episodes. In order to address this issue, here we have studied the long-term PFC gene expression pattern and behavioral effects induced by a chronic mild stress (CMS) model and antidepressant treatment in mice. CMS was applied to mice for six weeks and imipramine (10mg/kg, i.p.) or saline treatment was administered for five weeks starting from the third week of CMS. Mice were sacrificed one month after CMS and following two weeks after the discontinuation of drug treatment and the PFC was dissected and prepared for gene (mRNA) and protein expression studies. Using the same experimental design, a separate group of mice was tested for anhedonia, recognition memory, social interaction and anxiety. CMS induced a long-term altered gene expression profile in the PFC that was partially reverted by imipramine. Specifically, the circadian rhythm signaling pathway and functions such as gene expression, cell proliferation, survival and apoptosis as well as neurological and psychiatric disorders were affected. Of these, some changes of the circadian rhythm pathway (Hdac5, Per1, and Per2) were validated by RT-PCR and western-blot. Moreover, CMS induced long-lasting anhedonia that was reverted by imipramine treatment. Impaired memory, decreased social interaction and anxiety behavior were also induced by chronic stress. We have identified in the PFC molecular targets oppositely regulated by CMS and imipramine that could be relevant for chronic depression and antidepressant action. Among these, a possible candidate for further investigation could be the circadian rhythm pathway. |
| File Format | HTM / HTML |
| ISSN | 00913057 |
| Volume Number | 135 |
| e-ISSN | 18735177 |
| Journal | Pharmacology Biochemistry and Behavior |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2015-08-01 |
| Publisher Place | United States |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Discipline Behavioral Sciences Discipline Biochemistry Discipline Pharmacology Antidepressive Agents, Tricyclic Pharmacology Behavior, Animal Drug Effects Gene Expression Imipramine Prefrontal Cortex Metabolism Stress, Psychological Genetics Psychology Anhedonia Animals Anxiety Circadian Rhythm Histone Deacetylases Biosynthesis Interpersonal Relations Male Memory Mice Mice, Inbred C57bl Rna, Messenger Recognition (psychology) Journal Article Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Biological Psychiatry Behavioral Neuroscience Biochemistry Clinical Biochemistry Toxicology Pharmacology |
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