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Olga Pe?agarikano和同事在一個自閉癥小鼠模型中證明，催產(chǎn)素可明顯地改善其社會行為，如果進(jìn)行早期治療，這一裨益可能長時間持續(xù)。

催產(chǎn)素是一種幫助動物建立社會關(guān)系和信任的激素;人們對將它作為一種可能的對自閉癥譜系障礙的治療產(chǎn)生了強(qiáng)烈興趣，但臨床試驗(yàn)迄今產(chǎn)生的是混雜的結(jié)果。

為了了解該激素如何在大腦中作用，研究人員通過刪除一個基因而創(chuàng)制了一種患遺傳型自閉癥的小鼠，它會引起包括自閉癥譜系障礙的遺傳性發(fā)育綜合癥。他們發(fā)現(xiàn)，接受催產(chǎn)素治療的自閉癥小鼠在行為測試上的表現(xiàn)會好得多，它們會比單獨(dú)小鼠花更多時間與其它小鼠互動。給這些小鼠一種可在腦中激發(fā)催產(chǎn)素釋放的藥物會產(chǎn)生相同的效果。解剖發(fā)現(xiàn)，患自閉癥小鼠的腦子顯示該激素水平較低，這是因?yàn)楫a(chǎn)生催產(chǎn)素的神經(jīng)元較少所致。

為了測試催產(chǎn)素是否能在神經(jīng)元回路還在形成中的早期發(fā)育時期影響這些小鼠，Pe?agarikano和同事在它們出生后不久每日用催產(chǎn)素治療這些自閉癥小鼠。早期治療可對小鼠的社交技能產(chǎn)生持久的裨益，它能在停止治療后持續(xù)一周以上。

這些結(jié)果支持對催產(chǎn)素作為可能治療某些形式的自閉癥進(jìn)行探索，并提示可能有一個關(guān)鍵的時間窗，在該時間窗內(nèi)，早期治療可幫助恢復(fù)社交能力。

原文鏈接：Exogenous and evoked oxytocin restores social behavior in the Cntnap2 mouse model of autism

Mouse models of neuropsychiatric diseases provide a platform for mechanistic understanding and development of new therapies. We previously demonstrated that knockout of the mouse homolog of CNTNAP2 (contactin-associated protein-like 2), in which mutations cause cortical dysplasia and focal epilepsy (CDFE) syndrome, displays many features that parallel those of the human disorder. Because CDFE has high penetrance for autism spectrum disorder (ASD), we performed an in vivo screen for drugs that ameliorate abnormal social behavior inCntnap2 mutant mice and found that acute administration of the neuropeptide oxytocin improved social deficits. We found a decrease in the number of oxytocin immunoreactive neurons in the paraventricular nucleus (PVN) of the hypothalamus in mutant mice and an overall decrease in brain oxytocin levels. Administration of a selective melanocortin receptor 4 agonist, which causes endogenous oxytocin release, also acutely rescued the social deficits, an effect blocked by an oxytocin antagonist. We confirmed that oxytocin neurons mediated the behavioral improvement by activating endogenous oxytocin neurons in the paraventricular hypothalamus with Designer Receptors Exclusively Activated by Designer Drugs (DREADD). Last, we showed that chronic early postnatal treatment with oxytocin led to more lasting behavioral recovery and restored oxytocin immunoreactivity in the PVN. These data demonstrate dysregulation of the oxytocin system in Cntnap2 knockout mice and suggest that there may be critical developmental windows for optimal treatment to rectify this deficit.