PMID- 28890399
OWN - NLM
STAT- MEDLINE
DCOM- 20180611
LR  - 20200930
IS  - 1872-7972 (Electronic)
IS  - 0304-3940 (Linking)
VI  - 660
DP  - 2017 Nov 1
TI  - Activated brain-derived neurotrophic factor/TrkB signaling in rat dorsal and 
      ventral hippocampi following 10-day electroconvulsive seizure treatment.
PG  - 45-50
LID - S0304-3940(17)30745-0 [pii]
LID - 10.1016/j.neulet.2017.09.011 [doi]
AB  - Electroconvulsive therapy (ECT) is still the most effective strategy to treat 
      severe and drug-resistant depressive disorders. Electroconvulsive seizure (ECS), 
      which induces neuroplastic structural alterations and resilient behavioral 
      changes in experimental animals, is the model of the ECT for human depression. 
      ECT is typically administered three times per week for up to 4 weeks, while ECS 
      treatments are administered daily for 10days. The increased expression of 
      hippocampal brain-derived neurotrophic factor (BDNF) induced by antidepressive 
      ECS treatment in experimental animals has been well documented. BDNF executes 
      various neuroplastic functions by phosphorylating its high-affinity receptor, 
      full-length TrkB, which has an intrinsic tyrosine kinase domain. However, the 
      exact activation of BDNF/TrkB signaling following multiple ECS treatments has not 
      been well elucidated. In epileptogenesis, conflicting effects of BDNF have been 
      reported; while acute BDNF administration enhanced neuronal hyperexcitability and 
      induced epileptiform activities, continuous BDNF infusion inhibited 
      epileptogenesis. These conflicting results have been attributed to 
      agonist-induced adaptive response of expressional down-regulation of the BDNF 
      receptor. In the present study, using western blotting, we demonstrated increased 
      phosphorylation as well as decreased expression of the full-length TrkB receptor 
      (145kD) in both dorsal and ventral hippocampal regions of rats after a 10-day ECS 
      treatment. The expression of mature BDNF (14kD) was up-regulated while that of 
      proBDNF (32kD) remained unaltered in both hippocampal regions after the ECS 
      treatment. Our results indicate that the hippocampal BDNF/TrkB signaling pathway 
      is activated by multiple ECS treatments despite the ligand-induced 
      down-regulation of the full-length TrkB receptor.
CI  - Copyright (c) 2017 Elsevier B.V. All rights reserved.
FAU - Enomoto, Shingo
AU  - Enomoto S
AD  - Department of Psychiatry, National Defense Medical College, Tokorozawa, Saitama, 
      Japan.
FAU - Shimizu, Kunio
AU  - Shimizu K
AD  - Division of Behavioral Sciences, National Defense Medical College, Tokorozawa, 
      Saitama, Japan.
FAU - Nibuya, Masashi
AU  - Nibuya M
AD  - Department of Psychiatry, Tohoku Medical and Pharmaceutical University, Sendai, 
      Miyagi, Japan. Electronic address: nibrin@hosp.tohoku-mpu.ac.jp.
FAU - Suzuki, Eiji
AU  - Suzuki E
AD  - Department of Psychiatry, Tohoku Medical and Pharmaceutical University, Sendai, 
      Miyagi, Japan.
FAU - Nagata, Kiyoshi
AU  - Nagata K
AD  - Department of Environmental and Health Science, Faculty of Pharmaceutical 
      Sciences, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan.
FAU - Kondo, Takashi
AU  - Kondo T
AD  - Department of Chest Surgery, Tohoku Medical and Pharmaceutical University, 
      Sendai, Miyagi, Japan.
LA  - eng
PT  - Journal Article
DEP - 20170907
PL  - Ireland
TA  - Neurosci Lett
JT  - Neuroscience letters
JID - 7600130
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - EC 2.7.10.1 (Ntrk2 protein, rat)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Electroconvulsive Therapy
MH  - *Electroshock
MH  - Hippocampus/*metabolism
MH  - Male
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/*metabolism
MH  - *Seizures
MH  - Signal Transduction
OTO - NOTNLM
OT  - Agonist-induced receptor down-regulation
OT  - Brain-derived neurotrophic factor
OT  - Electroconvulsive seizure
OT  - Electroconvulsive therapy
OT  - Phosphorylational activation
OT  - TrkB
EDAT- 2017/09/12 06:00
MHDA- 2018/06/12 06:00
CRDT- 2017/09/12 06:00
PHST- 2017/07/11 00:00 [received]
PHST- 2017/08/31 00:00 [revised]
PHST- 2017/09/06 00:00 [accepted]
PHST- 2017/09/12 06:00 [pubmed]
PHST- 2018/06/12 06:00 [medline]
PHST- 2017/09/12 06:00 [entrez]
AID - S0304-3940(17)30745-0 [pii]
AID - 10.1016/j.neulet.2017.09.011 [doi]
PST - ppublish
SO  - Neurosci Lett. 2017 Nov 1;660:45-50. doi: 10.1016/j.neulet.2017.09.011. Epub 2017 
      Sep 7.