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Therapeutic potential of glycine receptors in pain sensory pathways

甘氨酸受体在疼痛感觉通路中的治疗潜力

基本信息

批准号：
nhmrc : 455931
负责人：
Prof Joseph Lynch
金额：
$ 19.49万
依托单位：
The University of Queensland
依托单位国家：
澳大利亚
项目类别：
NHMRC Project Grants
财政年份：
2007
资助国家：
澳大利亚
起止时间：
2007-01-01 至 2009-12-31
项目状态：
已结题

来源：
https://researchdata.edu.au/therapeutic-potential-glycine-sensory-pathways/82353
关键词：
Therapeutic potential glycine receptors pain

项目摘要

Inflammation caused by infection or injury leads to a heightened sensation of pain and can convert non-painful stimuli (e.g., touch) into painful stimuli. This effect is mediated by the production of prostaglandins both in peripheral tissues and in the spinal cord. Prostaglandins have recently been shown to decrease the magnitude of the inhibitory neurotransmission that normally occurs onto pain sensing neurons in the spinal cord. This has the effect of raising the excitability of these neurons, thereby making it easier for weak pain stimuli to be relayed to the brain. Inhibitory neurotransmission onto pain sensing neurons is largely mediated by the alpha3 glycine receptor subunit that is not found anywhere else in the body. Very little is known about the physiological and pharmacological properties of these receptors. We hypothesise that drugs that increase the activation of alpha3 glycine receptors may provide a novel treatment for pain. This project will firstly identify new drugs that can increase the activation of these receptors. It will then test whether these drugs are likely to work in vivo. The project will also establish why these receptors are found only on pain neurons. Together, this information will establish whether alpha3 glycine receptors represent a promising new therapeutic target for inflammatory pain, and will place us in an excellent position to begin the next step of identifying novel therapeutic lead compounds.

由感染或损伤引起的炎症导致疼痛感增强，并且可以将非疼痛刺激（例如，触摸）到痛苦的刺激。这种作用是由外周组织和脊髓中的野牡丹素的产生介导的。前列腺素最近被证明可以降低抑制性神经传递的幅度，这种抑制性神经传递通常发生在脊髓中的痛觉神经元上。这具有提高这些神经元的兴奋性的效果，从而使弱疼痛刺激更容易传递到大脑。疼痛感受神经元上的抑制性神经传递主要由在身体其他任何地方都没有发现的α 3甘氨酸受体亚基介导。对这些受体的生理和药理学特性知之甚少。我们假设，增加α 3甘氨酸受体激活的药物可能提供一种新的疼痛治疗方法。该项目将首先确定可以增加这些受体激活的新药。然后将测试这些药物是否可能在体内起作用。该项目还将确定为什么这些受体只在疼痛神经元上发现。总之，这些信息将确定α 3甘氨酸受体是否代表一个有前途的新的治疗炎症疼痛的目标，并将使我们处于一个很好的位置，开始下一步确定新的治疗先导化合物。