Cruz Dianne A, Eggan Stephen M, Azmitia Efrain C, Lewis David A
Department of Psychiatry, University of Pittsburgh, PA 15213, USA.
Am J Psychiatry. 2004 Apr;161(4):739-42. doi: 10.1176/appi.ajp.161.4.739.
Inhibition mediated by gamma-aminobutyric acid at the axon initial segment of pyramidal neurons appears to be altered in the prefrontal cortex in schizophrenia. This study examined the densities and laminar distribution of axon initial segments labeled with an antibody against the serotonin(1A) (5-HT(1A)) receptor, which also mediates inhibitory regulation of pyramidal neurons, in subjects with schizophrenia.
The densities and laminar distribution of axon initial segments with 5-HT(1A)-like immunoreactivity were assessed in postmortem tissue from the prefrontal cortex (Brodmann's area 46) of 14 matched triads of subjects with schizophrenia, subjects with major depressive disorder, and comparison subjects with no psychiatric disorder.
The relative densities of the labeled axon initial segment in both the superficial and the deep cortical layers did not differ across the three subject groups.
The findings do not support a role for altered serotonin transmission by means of the 5-HT(1A) receptor in dysfunction of prefrontal cortex pyramidal neurons in schizophrenia.
在精神分裂症患者中，γ-氨基丁酸在锥体神经元轴突起始段介导的抑制作用似乎在前额叶皮质发生了改变。本研究检测了用抗5-羟色胺（1A）（5-HT（1A））受体抗体标记的轴突起始段的密度和层状分布，该受体也介导锥体神经元的抑制性调节，研究对象为精神分裂症患者。
在14组匹配的三联体研究对象（精神分裂症患者、重度抑郁症患者和无精神疾病的对照对象）的前额叶皮质（布罗德曼46区）的尸检组织中，评估具有5-HT（1A）样免疫反应性的轴突起始段的密度和层状分布。
在三个研究对象组中，浅层和深层皮质层中标记的轴突起始段的相对密度没有差异。
这些发现不支持通过5-HT（1A）受体改变5-羟色胺传递在精神分裂症前额叶皮质锥体神经元功能障碍中起作用。
