Science· 2012Q1
Synaptic Dysfunction in Depression: Potential Therapeutic Targets
- 1,621citations
- Q1SCImago
- 2012year
Short summary
Ketamine rapidly reverses stress-induced synaptic deficits and produces antidepressant effects within hours, highlighting synaptogenesis as a key mechanism for mood regulation and treatment response.
AI-generated from the title and abstract; the full text is not read.
Key points
- Depression is associated with reduced neuronal synapses in the prefrontal cortex and hippocampus.
- Typical antidepressants have limited efficacy and delayed response times.
- Ketamine rapidly reverses synaptic deficits caused by chronic stress.
- Ketamine produces rapid antidepressant responses within hours, even in treatment-resistant patients.
- Synaptogenesis is proposed as a central mechanism for mood regulation and antidepressant treatment response.
AI-generated from the title and abstract; the full text is not read.
Abstract
Basic and clinical studies demonstrate that depression is associated with reduced size of brain regions that regulate mood and cognition, including the prefrontal cortex and the hippocampus, and decreased neuronal synapses in these areas. Antidepressants can block or reverse these neuronal deficits, although typical antidepressants have limited efficacy and delayed response times of weeks to months. A notable recent discovery shows that ketamine, a N-methyl-D-aspartate receptor antagonist, produces rapid (within hours) antidepressant responses in patients who are resistant to typical antidepressants. Basic studies show that ketamine rapidly induces synaptogenesis and reverses the synaptic deficits caused by chronic stress. These findings highlight the central importance of homeostatic control of mood circuit connections and form the basis of a synaptogenic hypothesis of depression and treatment response.
The authors' abstract, as published at the source. Science, 2012 · DOI ↗
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Field: Pharmacology (Medicine)
PharmacologyMedicine