2012年10月9日 訊 /生物谷BIOON/ --刊登在10月5日的國際雜志Science上的一篇研究報(bào)告中,，來自耶魯大學(xué)醫(yī)學(xué)院的研究者揭示了兒科麻醉劑可以幫助壓力和抑郁所致的損傷腦細(xì)胞進(jìn)行突觸的再生和重新連接,。
相比當(dāng)前別的抗抑郁藥物,，麻醉劑氯胺酮（Ketamine）可以對(duì)全身不同類型的神經(jīng)遞質(zhì)系統(tǒng)進(jìn)行作用,，理解氯胺酮如何在大腦中工作對(duì)于開發(fā)新型抗抑郁藥物可以提供新的思路和建議,，當(dāng)然這也是數(shù)百萬慢性抑郁癥患者的一大福音,。
氯胺酮的快速療效對(duì)于耐藥的抑郁癥患者來說非常好，氯胺酮的藥效可以維持一周至10天,，如果大劑量服用該藥物可以引發(fā)短期的精神異常等病癥,。
這項(xiàng)研究中,，研究者Duman揭示了,，氯胺酮可以靶向釋放神經(jīng)遞質(zhì)谷氨酸鹽，隨后刺激神經(jīng)元突觸的生長,，該藥物可以逆轉(zhuǎn)由于慢性壓力所致的神經(jīng)元突觸損傷,。未來研究中，研究者希望通過深入研究,，來開發(fā)出可以復(fù)制氯胺酮療效的新型藥物來治療抑郁癥患者,。（生物谷Bioon.com）
編譯自：How Ketamine Defeats Chronic Depression
doi:10.1126/science.1222939
PMC:
PMID:
Synaptic Dysfunction in Depression: Potential Therapeutic Targets
Ronald S. Duman*, George K. Aghajanian
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.
