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Zhejiang Da Xue Xue Bao Yi Xue Ban.
2020 Aug 25; 49(4): 508–513.
Chinese.
doi:
10.3785/j.issn.1008-9292.2020.08.10
PMCID:
PMC8800729
PMID:
32985165
γ-氨基丁酸能中间神经元与自闭症谱系障碍的研究进展
Advances on GABAergic interneurons in autism spectrum disorders
Jianhong LUO
1 浙江大学医学院脑科学与脑医学系, 浙江 杭州 310058 1 浙江大学医学院脑科学与脑医学系, 浙江 杭州 310058 2 浙江大学医学院附属儿童医院, 浙江 杭州 310052
罗建红(1958-), 男, 博士, 教授, 博士生导师, 主要从事神经生物学研究; E-mail:
nc.ude.ujz@gnohnaijoul
;
https://orcid.org/0000-0001-7832-496X
nc.ude.ujz@54581712
https://orcid.org/0000-0002-0132-1848
第一作者：李杰(1995-), 男, 硕士研究生, 主要从事神经生物学研究; E-mail: ;
+
channel can enhance the action potential of GABAergic interneurons by reducing the inactivation of Na
+
channel. NMDA receptor, as a potential therapeutic target of ASD, can restore the NMDA function of GABAergic interneurons, which would be used to treat behavioral defects. In addition, there are many ion channels and receptors on GABAergic interneurons related to ASD. This article reviews GABAergic interneurons in the pathogenesis of ASD and the related interventions.
Keywords:
Autism spectrum disorders, Cortex, GABAergic neurons, Ion channels, Receptors
自闭症谱系障碍(autism spectrum disorders，ASD)是一类复杂的神经发育疾病，核心症状包括社交和互动功能障碍、重复刻板的行为以及狭窄兴趣 ，目前尚无行之有效的靶向治疗方法。ASD的遗传度很高，许多突触功能相关的基因突变(如 Shank3 、 Neuroligins 和 Neurexin 等)或拷贝数异常均会导致ASD 。从发病机制上看，基因的改变并不直接影响ASD患者的行为，而是在发育中引起神经元功能和突触的分子信号通路变化，然后在系统水平上影响大脑的环路功能直至行为表型。
γ-氨基丁酸能中间神经元是通过释放γ-氨基丁酸激活下游神经元的γ-氨基丁酸受体，使氯离子内流，从而达到抑制效果的一类神经元。γ-氨基丁酸能中间神经元的功能包括参与基本的微环路功能，如前馈、反馈抑制和γ振荡以及发育过程中脑皮层环路的形成。根据不同的分子标记，γ-氨基丁酸能神经元可以分为钙结合蛋白小清蛋白(parvalbumin，PV)中间神经元、神经肽生长抑素(somatostatin，SST)中间神经元和血管肠肽(vasoactive intestinal peptide，VIP)中间神经元这三种主要亚型 。PV中间神经元在新皮质中间神经元中占比近40%，由快速放电的篮状细胞和吊灯样细胞组成 ，接受来自丘脑和皮层的兴奋性输入，靶向调控兴奋性神经元，在皮层神经网络振荡中起重要作用 。SST中间神经元在中间神经元中的占比约30%，包括马蒂诺蒂细胞(Martinotti cells)和专门锚定大脑皮层Ⅳ层的一类神经元 ，主要是特异性靶向兴奋性神经元的远端树突，具有较高的自发活动水平和低阈值的规律放电特性 。VIP中间神经元具有双束、双极和双簇状的细胞形态和非快速放电的特性，集中分布在大脑皮层Ⅱ和Ⅲ层，优先接受皮质传入纤维的刺激，主要抑制SST中间神经元 。每一种神经元都有其特有的输入-输出连接特性，在形态特性、基因表达谱、突触后目标、突触特征、发育史以及最终的回路和行为功能上具有不同程度的特异性 。有研究者在许多ASD动物模型中观察到γ-氨基丁酸能中间神经元障碍 ，因此γ-氨基丁酸能中间神经元异常与ASD的发病可能相关。本文讨论了γ-氨基丁酸能中间神经元功能异常在ASD发病中的作用、机制，及以相关环节为靶点的治疗手段的最新研究进展。
1 γ-氨基丁酸能中间神经元功能受损与自闭症谱系障碍
研究数据显示，约30%的ASD患儿患有癫痫，而30%的癫痫患儿(在三级癫痫门诊就诊的患儿)也符合ASD的诊断标准 ，因此ASD和癫痫可能具有共同的病理和生理学基础。神经系统的兴奋性与抑制性失衡(excitation/inhibition imbalance，E/I失衡)导致癫痫发作的观点已经得到广泛认可，且E/I失衡也已被证实是ASD最主要的神经生理学特征之一，并可能导致神经环路功能改变、交流受损、异常社交以及重复刻板的行为等核心症状 。有研究显示，前额叶皮层在调节社会认知和神经微环路的E/I平衡中起着关键作用 。在正常小鼠中通过光遗传学抑制内侧前额叶皮层(medial prefrontal cortex, mPFC)的γ-氨基丁酸能中间神经元会使其出现认知功能缺陷 。γ-氨基丁酸能抑制信号活性的改变可能导致神经环路失去平衡，并导致环路出现异常的高水平兴奋，所以γ-氨基丁酸能信号传递的中断可能是导致ASD发展的潜在机制
γ-氨基丁酸能中间神经元三种不同亚型的功能受损均会导致ASD发生。SST中间神经元的表达水平在ASD模型小鼠内侧前额叶中下降，可能是导致其社交兴趣降低的基础 ，而SST神经元数量减少会导致 BRINP1 基因敲除小鼠出现ASD样行为 。PV中间神经元功能障碍和数量减少同样与ASD有关 ，通过光遗传学增强抑制性PV中间神经元的兴奋性，能迅速挽救缺乏 CNTNAP2 的成年自闭症模型小鼠的社交行为缺陷和多动性 。此外，研究人员发现，与健康者相比，ASD患者VIP中间神经元上的基因表达下调，且差异表达最明显 ，提示ASD患者的VIP中间神经元功能可能受损。
以上研究提示，γ-氨基丁酸能中间神经元在微环路和神经网络的高级计算中起着至关重要的作用，与ASD发病机制密切相关。
2 基于γ-氨基丁酸能中间神经元的潜在治疗靶点
研究发现， NL3-R451C 基因敲入自闭症模型小鼠mPFC脑区的γ振荡失调、PV中间神经元的兴奋性降低，而在模型小鼠的mPFC脑区重新表达神经配蛋白3(neuroligin-3)或对PV中间神经元实施40 Hz/8 Hz偶联的光遗传学刺激能够逆转该模型小鼠的社交行为缺陷 Neuroligin-3 基因敲除雄性小鼠表现出社交能力缺陷，在PV中间神经元重新表达神经配蛋白能挽救其社会缺陷 。低剂量大麻二醇治疗可以改善Dravet综合征小鼠自闭症样的社交障碍，表型挽救与海马齿状回γ-氨基丁酸能中间神经元兴奋性的恢复有关
γ-氨基丁酸能中间神经元的功能与神经元上的离子通道和受体蛋白有关，因此通过靶向操纵γ-氨基丁酸能中间神经元上的离子通道(如钠通道)和受体蛋白并恢复其功能，可能对治疗ASD的认知障碍有帮助，γ-氨基丁酸能中间神经元可能成为未来ASD一个重要的治疗靶细胞。
2.1 钠通道
在ASD小鼠中，γ-氨基丁酸能中间神经元的快速放电特性受损，而通过恢复快速发放中间神经元的兴奋性可以拯救小鼠的社交缺陷 。电压门控钠通道与动作电位的起始和传播有关，其中电压门控钠通道Nav1.1在锥体细胞中低表达，在PV中间神经元的轴突起始节段高表达，对PV中间神经元的兴奋性有重要影响 。电压门控钠通道活性降低，会削弱γ-氨基丁酸能中间神经元兴奋性 。因此，电压门控钠通道可能是治疗ASD的一个重要靶点。
PV中间神经元Nav1.1功能受损的小鼠表现出多动症、社交趋新受损和空间记忆的改变，γ-氨基丁酸能神经传递也被损伤，小剂量的氯硝西泮(一种γ-氨基丁酸A型受体的阳性变构调节剂)可以挽救其异常社交行为和恐惧记忆缺陷 。钠通道激活剂由于毒性较大、不良反应较多，应用受到限制，而选择性激活Nav1.1的药物可能对ASD、癫痫、精神分裂症和阿尔茨海默病等神经发育类疾病更具治疗潜力 。新型电压门控钠通道正向调节剂Lu AE98134可以通过降低动作电位阈值，提高PV中间神经元的兴奋性，能使 Dlx5/6 基因突变小鼠的PV中间神经元的放电特性正常化，放电频率增加，放电持续时间和阈值降低 。一种小分子Nav1.1激活剂AA43279通过减弱钠通道的快速失活，以浓度依赖的方式增加Nav1.1介导的电流，增强了PV中间神经元的放电频率，并增加了锥体神经元记录的自发抑制突触后电流 。蜘蛛毒多肽Hm1a可在不影响兴奋性神经元放电的情况下，选择性激活Nav1.1，恢复Dravet综合征小鼠PV中间神经元的功能，这一发现为遗传性癫痫和ASD等神经遗传性疾病的药物开发提供了新的方向
2.2 α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)受体
PV中间神经元中AMPA受体丢失可能会损害其前馈抑制性输出，主要是含GluA4的AMPA受体，最终改变皮层网络的振荡 。吡仑帕奈是一种非竞争性AMPA受体拮抗剂，通过急性给药能挽救SYNGAP1单倍体缺失小鼠行为状态依赖性皮质γ振荡的稳态 ，可能对ASD的γ振荡受损也有帮助。
2.3 N-甲基-D-天冬氨酸(NMDA)受体
NMDA受体是谷氨酸门控离子通道的亚型，由两个GluN1亚基和两个GluN2亚基组成 。非竞争性NMDA受体拮抗剂如氯胺酮 、地佐环平(MK-801) 能有效降低前额叶皮层中PV中间神经元的活性，早期暴露在这些药物环境下可以在动物体复现神经发育障碍的认知缺陷 ，提示改善PV中间神经元上NMDA受体功能缺陷可能是ASD的潜在治疗靶点。
GluN2B-NMDA受体通过特异性地影响PV中间神经元促进E/I平衡，阻断GluN2B-NMDA受体会破坏依赖于这种平衡的功能，包括突触可塑性、γ振荡和记忆，GluN2B选择性拮抗剂Ro25-6981可以挽救长时程增强和γ振荡缺陷，而长期给药则可以诱导长时程增强的持续性恢复 。早期用NMDA受体激动剂D-环丝氨酸治疗幼年Grin2b+/C456Y小鼠可挽救幼年小鼠的NMDA受体电流和长时程增强，并改善成年小鼠的类焦虑行为 。降低GluN1亚基的表达可以破坏NMDA受体的发育功能，NMDA受体功能减退会导致E/I平衡丧失，锥体细胞内兴奋性增强，PV中间神经元被选择性破坏，GABA B 受体激动剂巴氯芬可以改善 GluN1 基因敲降小鼠的E/I平衡、γ信噪比和行为认知缺陷 。因此，以γ-氨基丁酸能中间神经元上NMDA受体亚单位组成为靶点的环路疗法可能为ASD提供新的治疗方法。
2.4 γ-氨基丁酸能受体
研究者在136例阿根廷ASD患者和150名健康对照者中，对GABA受体亚基基因 GABRA1 、 GABRG2 、 GABRB3 和 GABRD 的单核苷酸多态性进行了筛选，发现 GABRB3 可能通过与 GABRD 的相互作用参与ASD发病 。ASD患者大脑皮层中GAD65和GAD67表达以及γ-氨基丁酸A型和B型受体表达均降低 ，γ-氨基丁酸受体的表达水平可能与ASD神经环路异常及认知功能损伤有关。AT-富集相互作用域1B(AT-rich interactive domain 1B， Arid1b )基因的单倍缺失会导致ASD和智力障碍， Arid1b 基因敲除杂合子小鼠的神经节突起皮质γ-氨基丁酸能中间神经元数量减少，中间神经元祖细胞增殖减少，大脑皮层出现E/I失衡，通过γ-氨基丁酸A型受体正向调节剂氯硝西泮可以挽救 Arid1b 基因敲除杂合子小鼠异常的认知和社会行为
3 结语
综上所述，γ-氨基丁酸能中间神经元通过塑造大脑高级功能达到影响动物认知行为的水平，γ-氨基丁酸能中间神经元受损会影响神经环路的发育水平从而导致ASD等一系列神经发育障碍。一方面，可以通过特异性调控γ-氨基丁酸能中间神经元的离子通道及受体的功能，弥补其快速放电的特性，达到皮层E/I平衡，挽救ASD的异常行为；另一方面，也可以通过其他神经元对γ-氨基丁酸能中间神经元的激活或抑制，在整体水平改善ASD中的行为缺陷。除了药物作用于γ-氨基丁酸能中间神经元的靶点之外，还可以通过中间神经元移植和基因治疗γ-氨基丁酸能中间神经元的缺陷来治疗ASD。在中间神经元移植方面，将来自MGE细胞的野生型胚胎期中间神经元移植到新生 Pten (ASD相关基因)突变小鼠的mPFC，虽然会加剧过多的突触抑制，但可以挽救其社交行为 。基因治疗方面，腺相关病毒(adeno-associated virus，AAV)介导的转基因受到广泛关注，针对目前小分子药物治疗的不足，研究人员在新生小鼠脑脊髓液注射编码钠通道NaVb1亚单位的AAV-Navb1可过表达Navb1，从而减轻Scn1a +/- 小鼠的异常表型，并改善多种病理性内表型
神经科学技术的应用转化到临床面临着许多问题，γ-氨基丁酸能中间神经元的基本功能在临床应用前还需要进一步了解，但是随着光遗传学、单细胞测序和多细胞膜片钳电生理等各种新技术的出现以及与材料和工程等交叉学科的融合，对ASD中γ-氨基丁酸能中间神经元功能障碍的分子机制进行进一步的综合研究，γ-氨基丁酸能中间神经元的结构和功能会逐渐明朗化，开发针对ASD等神经发育障碍性疾病靶向疗法的希望也越大。
Funding Statement
浙江省自然科学基金（LD19H090002）；广东省重点领域研发计划（2019B030335001）
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