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Burst-firing patterns in the prefrontal cortex underlying the neuronal mechanisms of depression probed by antidepressants.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Guo, Fei Zhang, Qi Zhang, Bing Fu, Zhiwen Wu, Bin Huang, Chenggang Li, Yang
Description	Country affiliation: China Author Affiliation: Guo F ( Key Laboratory of Receptor Research, Shanghai Institute of Materia Medical, Chinese Academy of Sciences, Shanghai, 201203, China.)
Abstract	Major depressive disorder (MDD) is one of the leading causes of morbidity worldwide. Several antidepressants have been widely prescribed to treat patients with MDD. However, neuronal changes in brain function remain poorly understood. Based on the standard chronic mild stress (CMS) model of depression in mice, we investigated the neuronal mechanisms of the classic antidepressant, fluoxetine, and a new compound (termed YY-23 in this study) derived from furostanol saponin. The results showed that both fluoxetine and YY-23 normalized CMS-induced depressive-like behaviors. YY-23 caused antidepressant-like behaviors with a faster action than fluoxetine. In terms of in vivo neuronal activities, a CMS-induced decrease in spontaneous firing in burst of medial prefrontal cortex pyramidal neurons rather than ventral tegmental area (VTA) was reversed by the chronic administration of fluoxetine and YY-23. We also found that CMS-induced deficits in the expression of prefrontal brain-derived neurotrophic factor (BDNF) were also restored by chronically administering YY-23 and fluoxetine. In addition, chronic administration of fluoxetine rather than YY-23 resulted in an improvement of antidepressive-like behavior and a change of burst firing of VTA in control-housed animals, indicating that the pharmacological effects of YY-23 were specific to CMS-treated animals. Together, these data suggest that the burst-firing patterns of pyramidal cells may be a neural biomarker of depressive-like mice and antidepressant action. Furthermore, synaptic transmission and BDNF may contribute to the rapid antidepressant-like effects on depression.
File Format	HTM / HTML
ISSN	0953816X
Issue Number	10
Volume Number	40
e-ISSN	14609568
Journal	European Journal of Neuroscience
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2014-11-01
Publisher Place	France
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Neuroscience Depressive Disorder Drug Therapy Physiopathology Prefrontal Cortex Drug Effects Action Potentials Animals Antidepressive Agents Pharmacology Brain-derived Neurotrophic Factor Metabolism Chronic Disease Disease Models, Animal Fluoxetine Male Mice Pyramidal Cells Random Allocation Stress, Psychological Ventral Tegmental Area Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Neuroscience

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