Hippocampal neurokinin-1 receptor and brain-derived neurotrophic factor gene expression is decreased in rat models of pain and stress
Hippocampal neurokinin-1 receptor and brain-derived neurotrophic factor gene expression is decreased in rat models of pain and stress
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DOI：
10.1016/j.neuroscience.2005.04.002
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发表时间：
2005-01-01
期刊：
影响因子：
3.3
通讯作者：
McCarson, KE
中科院分区：
文献类型：
--
作者：
Duric, V;McCarson, KE
急性或慢性应激可改变海马结构，引起神经元损伤，并降低海马神经营养因子脑源性神经营养因子（BDNF）的水平。速激肽P物质及其神经激肽-1（NK-1）受体可能在处理伤害性刺激的神经元系统中发挥关键作用;它们在应激激活系统中的重要性最近已被NK-1受体拮抗剂的抗抑郁样作用所证实。然而，海马神经激肽受体和感觉系统中的神经激肽受体之间的功能相似性知之甚少，海马NK-1受体在慢性疼痛中的意义也是如此。因此，我们研究了制动应激或炎症刺激对大鼠海马NK-1受体和BDNF基因表达的影响。大鼠接受急性或慢性固定应激，或急性（福尔马林）或慢性（完全弗氏佐剂）炎症刺激。右后爪。随后，海马体积和比重进行了测量和NK-1受体和BDNF mRNA水平定量使用核糖核酸酶保护试验。结果显示，无论是应激还是疼痛都下调了海马中NK-1受体和BDNF基因的表达。疼痛或压力导致海马体积增加;这可能是由于水肿（比重降低）。因此，BDNF和NK-1受体基因可塑性可能反映了感觉激活或对神经元损伤的反应。这些数据可能提供了有用的标记物海马激活慢性疼痛，并建议慢性疼痛和抑郁症的潜在机制的相似性。(c)2005由Elsevier Ltd代表IBRO出版。
Acute or chronic stress can alter hippocampal structure, cause neuronal damage, and decrease hippocampal levels of the neurotrophin brain-derived neurotrophic factor (BDNF). The tachykinin substance P and its neurokinin-1 (NK-1) receptor may play a critical role in neuronal systems that process nociceptive stimuli; their importance in stress-activated systems has recently been demonstrated by the antidepressant-like actions of NK-1 receptor antagonists. However, the functional similarities between neurokinin receptors in the hippocampus and those in sensory systems are poorly understood, as is the significance of hippocampal NK-1 receptor in the context of chronic pain. Therefore, we investigated the effects of immobilization stress or inflammatory stimuli on NK-1 receptor and BDNF gene expression in the rat hippocampus. Rats received an acute or chronic immobilization stress, or an acute (formalin) or chronic (complete Freund's adjuvant) inflammatory stimulus to the. right hind paw. Subsequently hippocampal volume and specific gravity were measured and NK-1 receptor and BDNF mRNA levels quantified using ribonuclease protection assays. Results showed that either stress or pain down-regulates expression of both NK-1 receptor and BDNF genes in the hippocampus. Hippocampal volume was increased by either pain or stress; this may be due to edema (decreased specific gravity). Thus, BDNF and NK-1 receptor gene plasticity may reflect sensory activation or responses to neuronal injury. These data may provide useful markers of hippocampal activation during chronic pain, and suggest similarities in the mechanisms underlying chronic pain and depression. (c) 2005 Published by Elsevier Ltd on behalf of IBRO.