Glutamate decarboxylase65-immunoreactive terminals in cingulate and prefrontal cortices of schizophrenic and bipolar brain
Glutamate decarboxylase65-immunoreactive terminals in cingulate and prefrontal cortices of schizophrenic and bipolar brain
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DOI：
10.1016/s0891-0618(00)00105-8
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发表时间：
2000-12-01
影响因子：
2.8
通讯作者：
Williams, M
中科院分区：
文献类型：
--
作者：
Benes, FM;Todtenkopf, MS;Williams, M
近年来的尸检研究表明，精神分裂症和双相情感障碍患者的皮质边缘系统可能存在GABA能神经传递缺陷。为了探讨这种可能性，我们建立了谷氨酸脱羧酶（GAD（65））65 kdalton亚型的免疫定位方法，并应用于12名正常人（CON）、12名精神分裂症（SZ）和5名躁狂抑郁症（MD）患者的前扣带回（ACCx）和前额叶（PFCx）皮质。在严格盲法条件下，采用计算机辅助技术，测定各皮质区锥体（PNs）和非锥体（NPs）神经元及Ⅱ、Ⅲ、Ⅴ、Ⅵ层神经元内GAD（65）-IR终末的密度。对于SZ，未检测到与PN或NP接触的CAD（65）-IR端子的数密度或ACCx或PFCx中的层II-VI的NPL的差异。PN和NP的大小也没有差异，可能会影响这些结果的性质。使用像素计数分析，IR终端的大小，但是，被发现增加在第二层（10.3%）和第三层（15.8%）的SZ，但仅在受试者与精神安定药物治疗。对于MD，GAD（65）-IR终末的密度在ACCx的所有四层中均显著降低，但这些差异在第II层（27.8%）和第III层（37.2%）中最为显著，无论受试者是否接受了精神抑制剂治疗。在PFCx中，在检查的四个板层中，PN和NP的MD显示出类似的终末密度差异，但不显示神经元密度差异。MD组在细胞体大小和IR终末方面均无差异。年龄和PMI不能解释CON与SZ和MD之间的任何差异。总体而言，本研究的结果，虽然是初步的，表明可能有复杂的变化，在GABA能终端在SZ和MD，可能会有所不同，相对于初步诊断和抗精神病药物暴露。(C)2000 Elsevier Science B. V.保留所有权利。
Recent postmortem studies have been suggesting that a defect of GABAergic neurotransmission might occur in the corticolimbic system of subjects with schizophrenia and bipolar disorder. To explore this possibility, a method for immunolocalizing the 65 kdalton isoform of glutamate decarboxylase (GAD(65)) has been developed and applied to the anterior cingulate (ACCx) and prefrontal (PFCx) cortices of 12 normal controls (CONs), 12 schizophrenics (SZs) and 5 manic depressive (MDs) subjects. A computer-assisted technique was employed under strictly blind conditions to determine the density of GAD(65)-IR terminals in apposition with pyramidal (PNs) and nonpyramidal (NPs) neurons and in neuropil (NPL) of layers II, III, V and VI of each cortical region. For SZs, no difference in the numerical density of CAD(65)-IR terminals in contact with either PNs or NPs or in NPL of layers II-VI in ACCx or PFCx was detected. There were also no differences in the size of either PNs and NPs that could have influenced the nature of these findings. Using a pixel count analysis, the size of IR terminals was, however, found to be increased in layers II (10.3%) and III (15.8%) of SZs, but only in subjects treated with neuroleptic drugs. For MDs, the density of GAD(65)-IR terminals was significantly reduced in all four layers of ACCx, but these differences were most significant in layers II (27.8%) and III (37.2%), whether or not the subjected were treated with neuroleptics. Tn PFCx, the MDs showed similar differences in terminal density for PNs and NPs but not neuropil in the four laminae examined. The MD group showed no differences in either the size of cell bodies or IR terminals. Age and PMI did not account for any of the differences between the CONs vs SZs and MDs. Overall, the results of this study, though preliminary, suggest that there may be complex changes in GABAergic terminals in SZ and MD, ones that may vary with respect to primary diagnosis and neuroleptic exposure. (C) 2000 Elsevier Science B.V. All rights reserved.