Martínez-Mir M I, Pollard H, Moreau J, Traiffort E, Ruat M, Schwartz J C, Palacios J M
Departament de Farmacologia, Facultat de Medicina i Odontologia, Universitat de Valencia, Spain.
Synapse. 1993 Nov;15(3):209-20. doi: 10.1002/syn.890150306.
Autoradiographic techniques were used to study the distribution of histamine H2-receptors as labeled with [125I]iodoaminopotentidine in the brains of patients affected by human neurodegenerative pathologies, as compared with control cases. The highest levels of histamine H2 binding sites in control cases were found in the caudate, putamen, and accumbens nuclei. In Huntington's chorea, the levels of histamine H2-receptor binding sites were found to be markedly decreased in virtually all regions examined, particularly in the putamen and globus pallidus lateralis. The loss of binding sites was related to the grade of the disease. Losses were more marked in grade III disease cases. The possible influence of neuroleptic treatment, commonly used in Huntington's patients, was studied by including samples from clinically treated schizophrenic patients. A moderate increase in the densities of [125I]iodoaminopotentidine was found in the globus pallidus of these patients. In Parkinson's disease, the levels of histamine H2-receptor binding sites were found not to be significantly different from those of control cases. These results were comparable with those obtained from unilaterally neurotoxin-lesioned guinea pigs. Similar losses of binding sites were observed in the quinolinic acid lesioned striatal intrinsic neurons in the guinea pig, whereas lesioning dopaminergic cell bodies in the substantia nigra with 6-hydroxydopamine did not produce any significant change. These results strongly suggest that histamine H2-receptors are expressed by striatal neurons, which degenerate in Huntington's chorea, but not by nigral dopaminergic neurons and may play a role in the regulation of the intact striato-nigral pathway.
采用放射自显影技术,研究了[125I]碘氨基强痛定标记的组胺H2受体在人类神经退行性病变患者大脑中的分布,并与对照病例进行比较。对照病例中组胺H2结合位点水平最高的部位是尾状核、壳核和伏隔核。在亨廷顿舞蹈病中,几乎所有检测区域的组胺H2受体结合位点水平均显著降低,尤其是壳核和外侧苍白球。结合位点的丧失与疾病严重程度相关。在III级疾病病例中丧失更为明显。通过纳入临床治疗的精神分裂症患者样本,研究了亨廷顿病患者常用的抗精神病药物治疗的可能影响。在这些患者的苍白球中发现[125I]碘氨基强痛定密度有适度增加。在帕金森病中,组胺H2受体结合位点水平与对照病例相比无显著差异。这些结果与单侧神经毒素损伤的豚鼠获得的结果相当。在豚鼠喹啉酸损伤的纹状体内在神经元中观察到类似的结合位点丧失,而用6-羟基多巴胺损伤黑质中的多巴胺能细胞体未产生任何显著变化。这些结果强烈表明,组胺H2受体由亨廷顿舞蹈病中发生退化的纹状体神经元表达,而非由黑质多巴胺能神经元表达,并且可能在完整的纹状体-黑质通路调节中发挥作用。