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首页> 外文期刊>The European Journal of Neuroscience >Neurobiology of pain, interoception and emotional response: Lessons from nerve growth factor-dependent neurons
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Neurobiology of pain, interoception and emotional response: Lessons from nerve growth factor-dependent neurons

机译：疼痛的神经生物学，中生性和情绪反应：神经生长因子依赖性神经元的教训

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Although nerve growth factor (NGF) is a well-known neurotrophic factor, it also acts as a mediator of pain, itch and inflammation. Congenital insensitivity to pain with anhidrosis (CIPA) is an autosomal recessive genetic disorder caused by loss-of-function mutations in NTRK1, the gene encoding a receptor tyrosine kinase for NGF, TrkA. Mutations in NTRK1 cause the selective loss of NGF-dependent neurons in otherwise intact systems. NGF-dependent primary afferents are thinly myelinated Aδ or unmyelinated C-fibers that are dependent on the NGF-TrkA system during development. In CIPA, the lack of pain and the presence of anhidrosis (inability to sweat) are due to the absence of both NGF-dependent primary afferents and sympathetic postganglionic neurons, respectively. These peripheral neurons form an interface between the nervous system and the 'body-proper' and play essential roles in the interoception and sympathetic regulation of various tissues or organs. Patients with CIPA also show mental retardation and characteristic behaviors and are probably neuron-deficient within the brain. However, the functions of NGF-dependent neurons in the brain are controversial, both in animal and in human studies. This review focuses on various brain regions that express TrkA mRNA, based on data from the Allen Human Brain Atlas, and discusses putative neuronal networks related to these brain regions in humans. A better understanding the distribution of NGF-dependent neurons in the brain will provide a framework for further studies to investigate pain, interoception and emotional responses. Furthermore, strategies targeting the molecular mechanisms through which the NGF-TrkA system functions may provide hope for the development of novel analgesics.
机译：虽然神经生长因子（NGF）是着名的神经营养因子，但它也充当疼痛，瘙痒和炎症的介质。先天性对血管病（CIPA）疼痛的先天性不敏感是由NTRK1中的功能突变丧失引起的常染色体隐性遗传疾病，该基因编码NGF，TRKA的受体酪氨酸激酶。 NTRK1中的突变导致完整的系统中的NGF依赖性神经元的选择性丧失。 NGF依赖性初级传入较薄的弱肢体Aδ或非髓鞘C纤维，其在开发过程中依赖于NGF-TRKA系统。在CIPA中，缺乏疼痛和鼻腔的存在（无法出汗）是由于没有NGF依赖性发作和同情的柱状神经元。这些外周神经元在神经系统和“身体适当”之间形成界面，并在各种组织或器官的间歇性和交感神经调节中起着基本作用。患有CIPA的患者还表现出精神发育迟滞和特征行为，并且大脑内可能是神经元缺陷。然而，大脑中NGF依赖性神经元的功能是争议的，既是动物和人类研究。本综述重点介绍了以艾伦人脑图集的数据表达TRKA mRNA的各种大脑区域，并讨论了与人类的这些脑区相关的推定神经元网络。更好地理解大脑中NGF依赖性神经元的分布将为进一步研究提供框架，以调查疼痛，间歇性和情绪反应。此外，靶向NGF-TRKA系统功能的分子机制的策略可以为新型镇痛药提供的希望提供希望。

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