Srikiatkhachorn A, Govitrapong P, Limthavon C
Neuro- and Behavioural Biology Center, Mahidol University, Salaya, Nakornpathom, Thailand.
Headache. 1994 Jan;34(1):8-11. doi: 10.1111/j.1526-4610.1994.hed3401008.x.
Transformation of episodic migraine to chronic daily headache (so called transformed migraine) is now a well recognized phenomenon. Although several factors, i.e. analgesic overuse, increasing age, psychiatric disorders are reported to play some roles in this transformation, the precise cascade is still unclear. Further suppression of an already abnormal antinociceptive system with up-regulation of post-synaptic receptors is one of the possible explanation. In order to understand the mechanism underlying this condition, 5-HT2 serotonin receptors on platelets were assayed by the radioligand binding technique. Six transformed migraine patients (67.67 +/- 1.52 years) and seven healthy controls (72.86 +/- 1.82 years) were studied. [3H]-spiperone and ketanserin were used to determine the specific binding. We found a significant increase (P < 0.05) in the maximal receptor numbers (Bmax) on platelet membrane of the migraine patients when compared to the controls (64.31 +/- 11.06 and 39.96 +/- 5.42 fmol/mg protein, respectively), whereas the dissociation equilibrium constant (KD) values remained unchanged (3.63 +/- 0.78 nM and 2.84 +/- 0.48 nM for the migraine patients and controls, respectively). The up-regulation of serotonin receptors found in this study provided further support to the "serotonergic hypofunction" theory of migraine pathogenesis and may explain the unusual loss of episodicity seen in the transformed migraine patients.
发作性偏头痛转变为慢性每日头痛（即所谓的转化型偏头痛）如今是一种已得到充分认识的现象。尽管据报道有多种因素，如止痛药物过度使用、年龄增长、精神障碍等在这种转变中起了一定作用，但确切的发病过程仍不清楚。通过上调突触后受体进一步抑制原本就异常的抗伤害感受系统是一种可能的解释。为了了解这种病症的潜在机制，采用放射性配体结合技术检测了血小板上的5 - HT2血清素受体。研究了6例转化型偏头痛患者（年龄67.67±1.52岁）和7例健康对照者（年龄72.86±1.82岁）。使用[3H] - 螺哌隆和酮色林来测定特异性结合。我们发现，与对照组相比，偏头痛患者血小板膜上的最大受体数量（Bmax）显著增加（P < 0.05）（分别为64.31±11.06和39.96±5.42 fmol/mg蛋白质），而解离平衡常数（KD）值保持不变（偏头痛患者和对照组分别为3.63±0.78 nM和2.84±0.48 nM）。本研究中发现的血清素受体上调为偏头痛发病机制的“血清素功能减退”理论提供了进一步支持，并可能解释了转化型偏头痛患者发作性异常丧失的现象。
