PMID- 24296153
OWN - NLM
STAT- MEDLINE
DCOM- 20141203
LR  - 20140303
IS  - 1873-7064 (Electronic)
IS  - 0028-3908 (Linking)
VI  - 79
DP  - 2014 Apr
TI  - Effects of antidepressant drugs on synaptic protein levels and dendritic 
      outgrowth in hippocampal neuronal cultures.
PG  - 222-33
LID - S0028-3908(13)00565-0 [pii]
LID - 10.1016/j.neuropharm.2013.11.019 [doi]
AB  - The alteration of hippocampal plasticity has been proposed to play a critical 
      role in both the pathophysiology and treatment of depression. In this study, the 
      ability of different classes of antidepressant drugs (escitalopram, fluoxetine, 
      paroxetine, sertraline, imipramine, tranylcypromine, and tianeptine) to mediate 
      the expression of synaptic proteins and dendritic outgrowth in rat hippocampal 
      neurons was investigated under toxic conditions induced by B27 deprivation, which 
      causes hippocampal cell death. Postsynaptic density protein-95 (PSD-95), 
      brain-derived neurotrophic factor (BDNF), and synaptophysin (SYP) levels were 
      evaluated using Western blot analyses. Additionally, dendritic outgrowth was 
      examined to determine whether antidepressant drugs affect the dendritic 
      morphology of hippocampal neurons in B27-deprived cultures. Escitalopram, 
      fluoxetine, paroxetine, sertraline, imipramine, tranylcypromine, and tianeptine 
      significantly prevented B27 deprivation-induced decreases in levels of PSD-95, 
      BDNF, and SYP. Moreover, the independent application of fluoxetine, paroxetine, 
      and sertraline significantly increased levels of BDNF under normal conditions. 
      All antidepressant drugs significantly increased the total outgrowth of 
      hippocampal dendrites under B27 deprivation. Specific inhibitors of 
      calcium/calmodulin kinase II (CaMKII), KN-93, protein kinase A (PKA), H-89, or 
      phosphatidylinositol 3-kinase (PI3K), LY294002, significantly decreased the 
      effects of antidepressant drugs on dendritic outgrowth, whereas this effect was 
      observed only with tianeptine for the PI3K inhibitor. Taken together, these 
      results suggest that certain antidepressant drugs can enhance synaptic protein 
      levels and encourage dendritic outgrowth in hippocampal neurons. Furthermore, 
      effects on dendritic outgrowth likely require CaMKII, PKA, or PI3K signaling 
      pathways. The observed effects may be may be due to chronic treatment with 
      antidepressant drugs.
CI  - Copyright (c) 2013 Elsevier Ltd. All rights reserved.
FAU - Seo, Mi Kyoung
AU  - Seo MK
AD  - Paik Institute for Clinical Research, Inje University, Busan, Republic of Korea.
FAU - Lee, Chan Hong
AU  - Lee CH
AD  - Paik Institute for Clinical Research, Inje University, Busan, Republic of Korea.
FAU - Cho, Hye Yeon
AU  - Cho HY
AD  - Paik Institute for Clinical Research, Inje University, Busan, Republic of Korea.
FAU - Lee, Jung Goo
AU  - Lee JG
AD  - Paik Institute for Clinical Research, Inje University, Busan, Republic of Korea; 
      Department of Psychiatry, School of Medicine, Haeundae Paik Hospital, Republic of 
      Korea; Department of Health Science and Technology, Graduate School of Inje 
      University, Busan, Republic of Korea.
FAU - Lee, Bong Ju
AU  - Lee BJ
AD  - Department of Psychiatry, School of Medicine, Haeundae Paik Hospital, Republic of 
      Korea.
FAU - Kim, Ji Eun
AU  - Kim JE
AD  - Department of Psychiatry, School of Medicine, Haeundae Paik Hospital, Republic of 
      Korea.
FAU - Seol, Wongi
AU  - Seol W
AD  - InAm Neuroscience Research Center, Wonkwang University, Sanbon Hospital, Gunpo, 
      Republic of Korea.
FAU - Kim, Young Hoon
AU  - Kim YH
AD  - Paik Institute for Clinical Research, Inje University, Busan, Republic of Korea; 
      Department of Psychiatry, School of Medicine, Haeundae Paik Hospital, Republic of 
      Korea; Department of Health Science and Technology, Graduate School of Inje 
      University, Busan, Republic of Korea. Electronic address: neuro109@hanmail.net.
FAU - Park, Sung Woo
AU  - Park SW
AD  - Paik Institute for Clinical Research, Inje University, Busan, Republic of Korea; 
      Department of Health Science and Technology, Graduate School of Inje University, 
      Busan, Republic of Korea. Electronic address: swpark@inje.ac.kr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131201
PL  - England
TA  - Neuropharmacology
JT  - Neuropharmacology
JID - 0236217
RN  - 0 (Antidepressive Agents)
RN  - 0 (Antidepressive Agents, Second-Generation)
RN  - 0 (Antidepressive Agents, Tricyclic)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Thiazepines)
RN  - 01K63SUP8D (Fluoxetine)
RN  - 0DHU5B8D6V (Citalopram)
RN  - 0T493YFU8O (tianeptine)
RN  - 3E3V44J4Z9 (Tranylcypromine)
RN  - 41VRH5220H (Paroxetine)
RN  - OGG85SX4E4 (Imipramine)
RN  - QUC7NX6WMB (Sertraline)
SB  - IM
MH  - Animals
MH  - Antidepressive Agents/*pharmacology
MH  - Antidepressive Agents, Second-Generation/pharmacology
MH  - Antidepressive Agents, Tricyclic/pharmacology
MH  - Cell Enlargement/drug effects
MH  - Cells, Cultured
MH  - Citalopram/pharmacology
MH  - Dendrites/*drug effects/physiology
MH  - Fluoxetine/pharmacology
MH  - Hippocampus/*drug effects/physiology
MH  - Imipramine/pharmacology
MH  - Nerve Tissue Proteins/*drug effects
MH  - Neurons/*drug effects/physiology
MH  - Paroxetine/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sertraline/pharmacology
MH  - Thiazepines/pharmacology
MH  - Tranylcypromine/pharmacology
OTO - NOTNLM
OT  - Antidepressant drugs
OT  - Dendritic outgrowth
OT  - Hippocampal plasticity
OT  - Signaling
OT  - Synaptic proteins
EDAT- 2013/12/04 06:00
MHDA- 2014/12/15 06:00
CRDT- 2013/12/04 06:00
PHST- 2013/04/08 00:00 [received]
PHST- 2013/11/07 00:00 [revised]
PHST- 2013/11/21 00:00 [accepted]
PHST- 2013/12/04 06:00 [entrez]
PHST- 2013/12/04 06:00 [pubmed]
PHST- 2014/12/15 06:00 [medline]
AID - S0028-3908(13)00565-0 [pii]
AID - 10.1016/j.neuropharm.2013.11.019 [doi]
PST - ppublish
SO  - Neuropharmacology. 2014 Apr;79:222-33. doi: 10.1016/j.neuropharm.2013.11.019. 
      Epub 2013 Dec 1.