Publication Date:
2012-10-09
Description:
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.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4424898/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉 〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4424898/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duman, Ronald S -- Aghajanian, George K -- R01 MH093897/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 5;338(6103):68-72. doi: 10.1126/science.1222939.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Yale University School of Medicine, 34 Park Street, New Haven, CT 06508, USA. ronald.duman@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23042884" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Antidepressive Agents/*administration & dosage
;
Atrophy/pathology
;
Behavior/drug effects
;
Depressive Disorder, Major/*drug therapy/pathology/*physiopathology
;
Homeostasis/drug effects
;
Humans
;
Mice
;
Neurons/pathology
;
Stress, Psychological/pathology/physiopathology
;
Synapses/*drug effects/pathology/*physiology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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