PMID- 25209309
OWN - NLM
STAT- MEDLINE
DCOM- 20150723
LR  - 20141117
IS  - 1460-9568 (Electronic)
IS  - 0953-816X (Linking)
VI  - 40
IP  - 10
DP  - 2014 Nov
TI  - Burst-firing patterns in the prefrontal cortex underlying the neuronal mechanisms 
      of depression probed by antidepressants.
PG  - 3538-47
LID - 10.1111/ejn.12725 [doi]
AB  - 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.
CI  - (c) 2014 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.
FAU - Guo, Fei
AU  - Guo F
AD  - Key Laboratory of Receptor Research, Shanghai Institute of Materia Medical, 
      Chinese Academy of Sciences, Shanghai, 201203, China.
FAU - Zhang, Qi
AU  - Zhang Q
FAU - Zhang, Bing
AU  - Zhang B
FAU - Fu, Zhiwen
AU  - Fu Z
FAU - Wu, Bin
AU  - Wu B
FAU - Huang, Chenggang
AU  - Huang C
FAU - Li, Yang
AU  - Li Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140911
PL  - France
TA  - Eur J Neurosci
JT  - The European journal of neuroscience
JID - 8918110
RN  - 0 (Antidepressive Agents)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 01K63SUP8D (Fluoxetine)
SB  - IM
MH  - Action Potentials/drug effects
MH  - Animals
MH  - Antidepressive Agents/pharmacology
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Chronic Disease
MH  - Depressive Disorder/*drug therapy/*physiopathology
MH  - Disease Models, Animal
MH  - Fluoxetine/pharmacology
MH  - Male
MH  - Mice
MH  - Prefrontal Cortex/*drug effects/*physiopathology
MH  - Pyramidal Cells/drug effects/physiopathology
MH  - Random Allocation
MH  - Stress, Psychological
MH  - Ventral Tegmental Area/drug effects/physiopathology
OTO - NOTNLM
OT  - brain-derived neurotrophic factor
OT  - medial prefrontal cortex
OT  - mouse
OT  - ventral tegmental area
EDAT- 2014/09/12 06:00
MHDA- 2015/07/24 06:00
CRDT- 2014/09/12 06:00
PHST- 2014/02/26 00:00 [received]
PHST- 2014/08/15 00:00 [revised]
PHST- 2014/08/15 00:00 [accepted]
PHST- 2014/09/12 06:00 [entrez]
PHST- 2014/09/12 06:00 [pubmed]
PHST- 2015/07/24 06:00 [medline]
AID - 10.1111/ejn.12725 [doi]
PST - ppublish
SO  - Eur J Neurosci. 2014 Nov;40(10):3538-47. doi: 10.1111/ejn.12725. Epub 2014 Sep 
      11.