Phenotypes of pain behavior in phospholipase C-related but catalytically inactive protein type 1 knockout mice.
Phenotypes of pain behavior in phospholipase C-related but catalytically inactive protein type 1 knockout mice.
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DOI：
10.1186/1744-8069-7-79
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发表时间：
2011-10-18
期刊：
影响因子：
3.3
通讯作者：
Ueno S
中科院分区：
文献类型：
--
作者：
Migita K;Tomiyama M;Yamada J;Fukuzawa M;Kanematsu T;Hirata M;Ueno S
磷脂酶C相关失活蛋白（Phospholipase C-related inactive protein，PRIP）在GABAA受体转运至质膜中起重要作用，GABAA受体参与脊髓内显性抑制性神经传递，在伤害性信息传递中起重要作用。然而，PRIP在疼痛感觉中的作用仍然未知。在这项研究中，我们研究了PRIP 1型基因敲除（PRIP-1 -/-）小鼠的疼痛行为表型。与野生型小鼠相比，突变小鼠在福尔马林试验和von Frey试验的第二阶段中表现出痛觉过敏反应。GABAA受体的原位杂交研究显示PRIP-1 -/-小鼠脊髓背角和腹角γ2亚单位mRNA表达显著降低，而α1亚单位mRNA表达无差异。在PRIP-1 -/-小鼠脊髓的所有区域中，β2亚基mRNA表达显著高于野生型小鼠。另一方面，在野生型小鼠中，地西泮治疗显著增加了自发抑制电流的缓慢衰减时间常数，但在PRIP-1 -/-小鼠中没有增加。这些结果提示PRIP-1 -/-小鼠脊髓GABAA受体功能和亚单位表达的改变可能是导致PRIP-1-/-小鼠痛觉异常的重要原因。
Phospholipase C-related inactive protein (PRIP) plays important roles in trafficking to the plasma membrane of GABAA receptor, which is involved in the dominant inhibitory neurotransmission in the spinal cord and plays an important role in nociceptive transmission. However, the role of PRIP in pain sensation remains unknown. In this study, we investigated the phenotypes of pain behaviors in PRIP type 1 knockout (PRIP-1 -/- ) mice. The mutant mice showed hyperalgesic responses in the second phase of the formalin test and the von Frey test as compared with those in wild-type mice. In situ hybridization studies of GABAA receptors revealed significantly decreased expression of γ2 subunit mRNA in the dorsal and ventral horns of the spinal cord in PRIP-1 -/- mice, but no difference in α1 subunit mRNA expression. β2 subunit mRNA expression was significantly higher in PRIP-1 -/- mice than in wild-type mice in all areas of the spinal cord. On the other hand, the slow decay time constant for the spontaneous inhibitory current was significantly increased by treatment with diazepam in wild-type mice, but not in PRIP-1 -/- mice. These results suggest that PRIP-1 -/- mice exhibit the changes of the function and subunits expression of GABAA receptor in the spinal cord, which may be responsible for abnormal pain sensation in these mice.
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3.3
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