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感觉神经元特异性受体对伤害性信息传递的调制作用的研究

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目录

前言

声明

摘要

中文文摘

Chapter 1 Literature review

1.1. Sensory Neuron-specific Receptor

1.1.1. The Unique Location of SNSR

1.1.2. Functional characteristics of SNSR

1.1.3. The Prospect

1.2. Glutamate Receptors

1.2.1. The iGluR

1.2.2. The NMDA receptors

1.2.3. The mGluR

1.2.4. The Prospect

Chapter 2 INTRATHECAL SENSORY NEURON-SPECIFIC RECEPTOR AGONISTS BOVINE ADRENAL MEDULLA 8-22 AND (Tyr6) -γ2-MSH-6-12 INHIBIT FORMALIN-EVOKED NOCICEPTION AND NEURONAL Fos-LIKE IMMUNOREACTIVITY IN THE SPINAL CORD OF THE RAT

2.1. Methods

2.1.1. Animals

2.1.2. Drugs

2.1.3. Implantation of i.t. catheter

2.1.4. Formalin test

2.1.5. Histochemistry study

2.1.6. Data analysis

2.2. RESULTS

2.2.1. Effect of i.t. pretreatment with BAM8-22 on nocifensive response to i.pl.formalin

2.2.2. Effect of i.t. pretreatment with BAM8-22 on nocifensive response to i.pl.formalin in the presence of naloxone

2.2.3. Effect of i.t. post-treatment with BAM8-22 and MSH on nocifensive response to i.pl. formalin

2.2.4. Effects of i.t. BAM8-22 on formalin-evoked FLI expression in spinal cord in the absence and presence of naloxone

2.2.5. Effect of i.t. post-treatment with MSH on formalin-evoked FLI expression in spinal cord

2.3. Discussion

Chapter 3 INTRATHECAL SENSORY NEURON-SPECIFIC RECEPTOR AGONISTS BOVINE ADRENAL MEDULLA 8-22 AND (Tyr6)γ2-MSH-6-12 INHIBIT NMDA-EVOKED HYPERALGESIA AND ACTIVITY of DORSAL HORN NEURONS

3.1. Methods

3.1.1. Drugs

3.1.2. Nociceptive test

3.1.3. Spontaneous pain behavior

3.1.4. Histochemistry study

3.1.5. Data analysis

3.2. Results

3.2.1. Effect of i.t.pretreatment with BAM8-22 and MSH on NMDA-evoked-nocifensive response

3.2.2. Effect of i.t. pretreatment with BAM8-22 and MSH on NMDA-evoked hyperalgesia

3.2.3. Effects of i.t. SNSR agonists on NMDA-evoked FLI expression in spinal cord

3.3. Discussion

Reference List

攻读学位期间承担的科研任务与主要成果

Acknowledgments

Appendix

个人简历

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摘要

感觉神经元特异性受体(sensory neuron—specific receptor,SNSR)的基因仅仅在背根神经节和三叉神经节的小型神经元中表达。由于这些神经元是伤害性信息传递的初级神经元,推测SNSR受体的生理功能可能和伤害性信息传递的调制有关。我们采用福尔马林痛检验作为疼痛模型,观察牛肾上腺髓质肽8-22(Bovine adrenal medulla 8-22,BAM8-22)和Tyr6-γ2-MSH-6-12这两种SNSR受体的选择性激动剂对足底注射福尔马林所引起的疼痛反应以及脊髓背角C-fos蛋白表达的抑制作用,揭示SNSR受体的生理功能;同时还研究了这两种激动剂对N-甲基-D型-天冬氨酸(NMDA)引起的痛觉过敏的作用。实验结果显示:在福尔马林检验中,前处理(BAM8-22)和后处理(BAM8-22和MSH)均能显著减少疼痛反应,并能减少由疼痛引起的脊髓背角C-fos蛋白的表达。而BAM8-22和MSH前处理也能抑制由NMDA引起的痛觉过敏。这些结果证实激活脊髓背角的SNSR受体能抑制伤害性信息的传递,而这种抑制作用至少有部分是通过抑制NMDA受体实现的。

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