Cortical cholinergic dysfunction after human head injury
Cortical cholinergic dysfunction after human head injury
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DOI：
10.1089/neu.1998.15.295
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发表时间：
1998-05-01
影响因子：
4.2
通讯作者：
Dewar, D
中科院分区：
文献类型：
--
作者：
Murdoch, I;Perry, EK;Dewar, D
胆碱能神经传递的丧失与头部受伤后的记忆障碍和认知功能障碍有关。本研究的目的是调查突触前标记，特别是与头部受伤死亡患者和年龄匹配对照的人类死后大脑中胆碱能神经传递相关的标记。对 16 名头部受伤患者和 8 名对照者的颞下回、扣带回和顶上皮层的胆碱乙酰转移酶活性和高亲和力烟碱受体结合位点进行了测定。在同一患者组的左侧扣带回中测定了突触素免疫反应性。在头部受伤组中，与对照组相比，每个皮质区域的胆碱乙酰转移酶活性持续降低。硬膜下血肿的存在和头部损伤后生存期的延长往往与胆碱乙酰转移酶活性降低有关。与胆碱乙酰转移酶活性显着降低相反，与对照患者相比，头部受伤患者的尼古丁受体结合没有变化。与对照组相比，头部受伤组扣带回的突触素免疫反应性降低了约 30% (p < 0.05)。胆碱乙酰转移酶活性与突触素免疫反应性的相关性表明，在头部受伤后死后的人脑中存在胆碱能突触前末梢的缺陷。
Loss of cholinergic neurotransmission is implicated in memory impairment and cognitive dysfunction after head injury. The aim of the present study was to investigate presynaptic markers, particularly in relation to cholinergic neurotransmission in human postmortem brain from patients who died following a head injury and age-matched controls. Choline acetyltransferase activity and high-affinity nicotinic receptor binding sites were assayed in the inferior temporal gyrus, cingulate gyrus, and superior parietal cortex of 16 head-injured patients and 8 controls. Synaptophysin immunoreactivity was determined in the left cingulate gyrus from the same patient groups. In the head-injured group, choline acetyltransferase activity was consistently reduced in each cortical region compared to control subjects. The presence of a subdural haematoma and a prolonged survival period after head injury tended to be associated with lower choline acetyltransferase activity. In contrast to the marked reduction in choline acetyltransferase activity, nicotine receptor binding was unchanged in head-injured compared to control patients. Synaptophysin immunoreactivity in the cingulate gyrus was reduced by approximately 30% (p < 0.05) in the head-injured group compared to controls. Correlation of choline acetyltransferase activity with synaptophysin immunoreactivity indicated there is a deficit of cholinergic presynaptic terminals in postmortem human brain following head injury.