Department of Neuropsychiatry, Fukushima Medical University School of Medicine, 1 Hikarigaoka, Fukushima City, Fukushima 960-1295, Japan.
Prog Neuropsychopharmacol Biol Psychiatry. 2011 Dec 1;35(8):1901-7. doi: 10.1016/j.pnpbp.2011.07.010. Epub 2011 Jul 28.
In patients with schizophrenia, various physical disorders are sometimes discovered only when they have reached a later and more severe stage. This phenomenon is believed to be caused, at least in part, by an increase in pain threshold. The gamma-aminobutyric acid (GABA)-ergic and glutamatergic systems in the rostral agranular insular cortex (RAIC) are thought to be involved in the regulation of pain threshold. However, no postmortem studies of the cerebral cortex have previously been published. Dopamine and cAMP-regulated phosphoprotein 32 kD (DARPP-32), which is involved in the GABAergic and glutamatergic systems, is considered to be crucial for elucidating the pathogenesis of schizophrenia. Using specific antibodies, we conducted immunohistochemical examinations of the RAIC in 10 subjects from a healthy control group, and 11 subjects from a schizophrenia group. The sex, age, and postmortem interval (PMI) of the schizophrenia group were matched to those of the healthy control group. We revealed that the density of DARPP-32-immunoreactive (IR) neurons in the II and III layers of the RAIC was significantly decreased (p<0.05) in the schizophrenia group compared with the healthy control group. Our findings could partially explain the molecular basis of the pain threshold abnormalities found in patients with schizophrenia.
在精神分裂症患者中，各种身体疾病有时只有在更晚期和更严重的阶段才会被发现。这种现象被认为至少部分是由于疼痛阈值增加所致。人们认为，头侧无颗粒岛叶皮质（RAIC）中的γ-氨基丁酸（GABA）能和谷氨酸能系统参与了疼痛阈值的调节。然而，以前没有关于大脑皮质的尸体研究发表过。多巴胺和 cAMP 调节的磷酸蛋白 32 kD（DARPP-32）参与 GABA 能和谷氨酸能系统，被认为对阐明精神分裂症的发病机制至关重要。使用特异性抗体，我们对 10 名健康对照组和 11 名精神分裂症组的 RAIC 进行了免疫组织化学检查。精神分裂症组的性别、年龄和死后间隔（PMI）与健康对照组相匹配。我们发现，与健康对照组相比，RAIC 的 II 和 III 层中的 DARPP-32 免疫反应性（IR）神经元的密度明显降低（p<0.05）。我们的发现可以部分解释精神分裂症患者疼痛阈值异常的分子基础。
