PMID- 18033145
OWN - NLM
STAT- MEDLINE
DCOM- 20080219
LR  - 20201019
IS  - 0013-7006 (Print)
IS  - 0013-7006 (Linking)
VI  - 33
IP  - 4 Pt 1
DP  - 2007 Sep
TI  - [ECT: from neuronal plasticity to mechanisms underlying antidepressant medication 
      effect].
PG  - 572-8
AB  - INTRODUCTION: Electroconvulsive therapy (ECT) is one of the most effective 
      treatments for depression. Although it has been used for over 60 years, the basis 
      for its therapeutic effect is still unknown. Structural plasticity within the 
      nervous system such as neurogenesis or mossy fiber sprouting could be involved in 
      the mechanisms underlying the antidepressant effect of several pharmacological 
      antidepressants. But what is the mechanism underlying ECT? LITERATURE FINDINGS: 
      Several methodological issues using magnetic resonance spectroscopy for humans 
      and rats found changes in neuronal metabolism during ECT. The levels of 
      N-Acetyl-Aspartate, an amino acid exclusively located in neurons, are increased 
      after ECT; choline, which is believed to represent membrane turn-over, increases 
      as well. These results are in good agreement with ECT induced structural 
      plasticity. Electroconvulsive seizures (ECS), an animal model of ECT, can enhance 
      neurogenesis, particularly in the hippocampal dentate gyrus. A series of seizures 
      increases neurogenesis more than a single shock. In the glucocorticoid paradigm 
      of depression, ECS can increase hippocampal neurogenesis. This suggests that 
      induction of neurogenesis might be implicated in the antidepressant mechanism of 
      ECT. DISCUSSION: As suggested by previous studies, Brain Derived Neurotrophic 
      Factor (BDNF) is supposed to play a critical role in the action of 
      antidepressants through neuronal plasticity. ECS increases the expression of 
      BDNF. The BDNF gene has four differentially regulated promoters that generate 
      four transcript forms. Studying the regulation of these transcript forms by 
      diverse classes of antidepressant therapeutics, including ECS, suggests that 
      diverse signalling mechanisms may be recruited to regulate BDNF transcripts. 
      Moreover, for ECS, these signalling mechanisms seem to differ from those 
      recruited by excitotoxic cell death phenomena, such as neuronal damage or 
      epileptic seizure models. CONCLUSION: These results indicate the participation of 
      neuronal plasticity to help account for the antidepressant effect of ECT. 
      However, this relationship is currently not clearly defined, particularly in 
      terms of causality, and will require future studies to unravel it.
FAU - Holtzmann, J
AU  - Holtzmann J
AD  - Departement de Psychiatrie, Hopital Sud, Centre Hospitalier Universitaire de 
      Grenoble, avenue de Kimberley, BP 338, 38434 Echirolles.
FAU - Polosan, M
AU  - Polosan M
FAU - Baro, P
AU  - Baro P
FAU - Bougerol, T
AU  - Bougerol T
LA  - fre
PT  - English Abstract
PT  - Journal Article
PT  - Review
TT  - ECT: de la neuroplasticite aux mecanismes d'action.
PL  - France
TA  - Encephale
JT  - L'Encephale
JID - 7505643
RN  - 0 (Antidepressive Agents)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 30KYC7MIAI (Aspartic Acid)
RN  - 997-55-7 (N-acetylaspartate)
RN  - N91BDP6H0X (Choline)
SB  - IM
MH  - Antidepressive Agents/*pharmacology/*therapeutic use
MH  - Aspartic Acid/analogs & derivatives/metabolism
MH  - Brain/*drug effects/*physiopathology
MH  - Brain-Derived Neurotrophic Factor/drug effects/metabolism
MH  - Choline/metabolism
MH  - Depressive Disorder, Major/*physiopathology/*therapy
MH  - Electroconvulsive Therapy/*methods
MH  - Exons/drug effects
MH  - Humans
MH  - Neuronal Plasticity/*drug effects
RF  - 13
EDAT- 2007/11/23 09:00
MHDA- 2008/02/20 09:00
CRDT- 2007/11/23 09:00
PHST- 2007/11/23 09:00 [pubmed]
PHST- 2008/02/20 09:00 [medline]
PHST- 2007/11/23 09:00 [entrez]
AID - S0013-7006(07)92055-2 [pii]
AID - 10.1016/s0013-7006(07)92055-2 [doi]
PST - ppublish
SO  - Encephale. 2007 Sep;33(4 Pt 1):572-8. doi: 10.1016/s0013-7006(07)92055-2.