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腾讯登录Bioll Psychiatry：研究发现靶向治疗抑郁症的新途径
| 导读 | 近日，一项发表于《生物精神病学》（<em>Biological Psychiatry</em>）杂志的研究中，来自耶鲁大学医学院的Elsayed和他的团队发现：成纤维细胞生长因子-2（FGF2）可以促进神经胶质细胞的增殖，并抑制其减少，从而增加胶质细胞的数量。
该研究的作者Ronald Duman 说“这项研究发现了一种靶向治疗抑郁症的新途径，我们可以通过促进胶质细胞... |
近日，一项发表于《生物精神病学》（<em>Biological Psychiatry</em>）杂志的研究中，来自耶鲁大学医学院的Elsayed和他的团队发现：成纤维细胞生长因子-2（FGF2）可以促进神经胶质细胞的增殖，并抑制其减少，从而增加胶质细胞的数量。
该研究的作者Ronald Duman 说“这项研究发现了一种靶向治疗抑郁症的新途径，我们可以通过促进胶质细胞的生成与维持，为神经元执行其功能提供良好的环境支持。”
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大脑影像学和尸检研究发现抑郁症患者的大脑内连接通路大量减少，情感调节相关脑区的连接功能受损。神经胶质细胞对神经元的生长与功能维持起重要支持作用，尸检病理报告显示抑郁症患者脑组织中神经胶质细胞明显减少。
既往研究已经证实抗抑郁药对大脑结构产生积极影响，从而改善抑郁症状，而这种积极影响在绝大程度上取决于它们促进大脑中生长因子水平升高的能力。
为探讨FGF2是否可以治疗抑郁症，研究者采用各种可以引起抑郁症状（绝望及快感缺失）的自然压力制作啮齿类动物抑郁模型，发现脑室内灌入FGF2可以恢复慢性压力所致的神经胶质细胞减少。数据显示抗抑郁药物通过增强FGF2的信号来促进胶质细胞增殖与功能。
“越深入抗抑郁药作用的生物学机制，越复杂，然而这种复杂使科学的力量更强大，我们可以发现抗抑郁药治疗的局限，从而去寻求更新、更有效的治疗途径”，《生物精神病学》的编辑，耶鲁大学医学院精神病学系的首席John Krystal评论。
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<img src="http://www.bioon.com/biology/UploadFiles/201208/2012081822424322.gif" alt="" width="113" height="149" border="0" hspace="0" />
<a title="" href="http://dx.doi.org/10.1016/j.biopsych.2012.03.003" target="_blank">doi:10.1016/j.biopsych.2012.03.003</a>
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<br/><strong>Antidepressant Effects of Fibroblast Growth Factor-2 in Behavioral and Cellular Models of Depression</strong><br/>
Maha Elsayed, Mounira Banasr, Vanja Duric, Neil M. Fournier, Pawel Licznerski, Ronald S. Duman
Background
Basic and clinical studies report that the expression of fibroblast growth factor-2 (FGF-2) is decreased in the prefrontal cortex (PFC) of depressed subjects or rodents exposed to stress and increased following antidepressant treatment. Here, we aim to determine if 1) FGF-2/fibroblast growth factor receptor (FGFR) signaling is sufficient and required for mediating an antidepressant response behaviorally and cellularly; and 2) if the antidepressant actions of FGF-2 are mediated specifically by the PFC.
Methods
The role of FGF-2 signaling in behavioral models of depression and anxiety was tested using chronic unpredictable stress (CUS)/sucrose consumption test (SCT), forced swim test (FST), and novelty suppressed feeding test (NSFT). We also assessed the number of bromodeoxyuridine labeled dividing glial cells in the PFC as a cellular index relevant to depression (i.e., decreased by stress and increased by antidepressant treatment).
Results
Chronic FGF-2 infusions (intracerebroventricular) blocked the deficit in SCT caused by CUS. Moreover, the response to antidepressant treatment in the CUS/SCT and FST was abolished upon administration of an inhibitor of FGFR activity, SU5402. These results are consistent with the regulation of proliferating cells in the PFC, a portion of which are of oligodendrocyte lineage. Lastly, subchronic infusions of FGF-2 into the PFC but not into the dorsal striatum produced antidepressant-like and anxiolytic-like effects on FST and NSFT respectively.
Conclusions
These findings demonstrate that FGF-2/FGFR signaling is sufficient and necessary for the behavioral, as well as gliogenic, actions of antidepressants and highlight the PFC as a brain region sensitive to the antidepressant actions of FGF-2.
<br/>来源：医脉通
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该研究的作者Ronald Duman 说“这项研究发现了一种靶向治疗抑郁症的新途径，我们可以通过促进胶质细胞的生成与维持，为神经元执行其功能提供良好的环境支持。”
<!--more-->
大脑影像学和尸检研究发现抑郁症患者的大脑内连接通路大量减少，情感调节相关脑区的连接功能受损。神经胶质细胞对神经元的生长与功能维持起重要支持作用，尸检病理报告显示抑郁症患者脑组织中神经胶质细胞明显减少。
既往研究已经证实抗抑郁药对大脑结构产生积极影响，从而改善抑郁症状，而这种积极影响在绝大程度上取决于它们促进大脑中生长因子水平升高的能力。
为探讨FGF2是否可以治疗抑郁症，研究者采用各种可以引起抑郁症状（绝望及快感缺失）的自然压力制作啮齿类动物抑郁模型，发现脑室内灌入FGF2可以恢复慢性压力所致的神经胶质细胞减少。数据显示抗抑郁药物通过增强FGF2的信号来促进胶质细胞增殖与功能。
“越深入抗抑郁药作用的生物学机制，越复杂，然而这种复杂使科学的力量更强大，我们可以发现抗抑郁药治疗的局限，从而去寻求更新、更有效的治疗途径”，《生物精神病学》的编辑，耶鲁大学医学院精神病学系的首席John Krystal评论。
<div id="ztload">
<div>
<div>
<img src="http://www.bioon.com/biology/UploadFiles/201208/2012081822424322.gif" alt="" width="113" height="149" border="0" hspace="0" />
<a title="" href="http://dx.doi.org/10.1016/j.biopsych.2012.03.003" target="_blank">doi:10.1016/j.biopsych.2012.03.003</a>
PMC:
PMID:
</div>
<div>
<br/><strong>Antidepressant Effects of Fibroblast Growth Factor-2 in Behavioral and Cellular Models of Depression</strong><br/>
Maha Elsayed, Mounira Banasr, Vanja Duric, Neil M. Fournier, Pawel Licznerski, Ronald S. Duman
Background
Basic and clinical studies report that the expression of fibroblast growth factor-2 (FGF-2) is decreased in the prefrontal cortex (PFC) of depressed subjects or rodents exposed to stress and increased following antidepressant treatment. Here, we aim to determine if 1) FGF-2/fibroblast growth factor receptor (FGFR) signaling is sufficient and required for mediating an antidepressant response behaviorally and cellularly; and 2) if the antidepressant actions of FGF-2 are mediated specifically by the PFC.
Methods
The role of FGF-2 signaling in behavioral models of depression and anxiety was tested using chronic unpredictable stress (CUS)/sucrose consumption test (SCT), forced swim test (FST), and novelty suppressed feeding test (NSFT). We also assessed the number of bromodeoxyuridine labeled dividing glial cells in the PFC as a cellular index relevant to depression (i.e., decreased by stress and increased by antidepressant treatment).
Results
Chronic FGF-2 infusions (intracerebroventricular) blocked the deficit in SCT caused by CUS. Moreover, the response to antidepressant treatment in the CUS/SCT and FST was abolished upon administration of an inhibitor of FGFR activity, SU5402. These results are consistent with the regulation of proliferating cells in the PFC, a portion of which are of oligodendrocyte lineage. Lastly, subchronic infusions of FGF-2 into the PFC but not into the dorsal striatum produced antidepressant-like and anxiolytic-like effects on FST and NSFT respectively.
Conclusions
These findings demonstrate that FGF-2/FGFR signaling is sufficient and necessary for the behavioral, as well as gliogenic, actions of antidepressants and highlight the PFC as a brain region sensitive to the antidepressant actions of FGF-2.
<br/>来源：医脉通
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