Indian Journal of PsychiatryIndian Journal of Psychiatry
Home | About us | Current Issue | Archives | Ahead of Print | Submission | Instructions | Subscribe | Advertise | Contact | Login 
    Users online: 748 Small font sizeDefault font sizeIncrease font size Print this article Email this article Bookmark this page
Search Again
 Back
 Table of Contents
 
 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Article Access Statistics
 Reader Comments
 Email Alert
 Add to My List
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed4127    
    Printed159    
    Emailed8    
    PDF Downloaded449    
    Comments [Add]    
    Cited by others 15    

Recommend this journal

 
PG CME
Year : 2010  |  Volume : 52  |  Issue : 4  |  Page : 378-386

How antidepressant drugs act: A primer on neuroplasticity as the eventual mediator of antidepressant efficacy


1 Department of Psychopharmacology, National Institute of Mental Health and Neurosciences, Bangalore, India
2 The Logos Centre for Cognitive Behavioural Therapy and Mental Health Promotion, Tees Esk and Wear Valley NHS Trust, County Hospital, Durham, United Kingdom

Correspondence Address:
Chittaranjan Andrade
Department of Psychopharmacology, National Institute of Mental Health and Neurosciences, Bangalore 560 029
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-5545.74318

Rights and Permissions

Depression is conventionally viewed as a state of chemical imbalance, and antidepressants are suggested to act through increasing monoaminergic neurotransmission. These views are currently considered simplistic. This article examines the animal and human literature on the neurohistological mechanisms underlying stress, depression and antidepressant treatment. Pathological stress and depression are associated with changes such as loss of dendritic spines, shrinkage of the dendritic tree and loss of synapses in the hippocampus and prefrontal cortex. There is also a decrease in glia. Apoptosis may occur under extreme circumstances. In contrast, there is increased dendritic arborization and synaptogenesis in the amygdala. Antidepressant treatment protects against and even reverses some but not all of these stress-induced neurohistological changes. Pathological stress results in an aberrant neuroplasticity response characterized by abnormally increased activity in the amygdala and by impaired functioning of the hippocampus, prefrontal cortex and downstream structures. This aberrant neuroplasticity response directly explains most of the clinical symptoms of depression. Antidepressant treatment protects against stress-induced pathoplastic neurohistological and neurocognitive changes. Antidepressant treatment also restores functional neuroplasticity in stressed organisms and, thereby, presumably, facilitates re-adaptation through learning and memory mechanisms. Thus, the stress-depression syndrome and the therapeutic and prophylactic efficacy of antidepressant treatments can be explained through a hardwiring analogy. In this context, glutamate is an important neurotransmitter.



[FULL TEXT] [PDF]*

        

Print this article         Email this article