Neuronal hypertrophy in the neocortex of patients with temporal lobe epilepsy
Neuronal hypertrophy in the neocortex of patients with temporal lobe epilepsy
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DOI：
10.1523/jneurosci.21-13-04789.2001
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发表时间：
2001-07-01
影响因子：
5.3
通讯作者：
Farrell, M
中科院分区：
文献类型：
--
作者：
Bothwell, S;Meredith, GE;Farrell, M
颞叶癫痫（TLE）中新皮层受累的潜在原因仍然是一个基本的和未解决的问题。磁共振成像显示了颞叶体积的显著损失，并且有人提出，由于神经元丢失，新皮层回路在功能上受到干扰。本研究使用基于设计的立体学来估计Brodmann’s区38的体积和细胞数量，该区域通常在颞叶前部切除术中被切除。对海马硬化症（HS）患者的新皮层进行了研究。结果令人惊讶地发现，TLE患者有明显的新皮质灰质萎缩，但没有神经元损失。与对照组相比，TLE标本的神经元也明显变大，树突树显得更稀疏，脊柱密度明显降低。因此，我们在TLE患者中发现的神经元密度增加可归因于大神经元占据比正常大脑小得多的体积。下层白质中的神经元体积也增加了，但与其他报道相反，在数量或密度上没有显著增加。神经元肥大对HS和非HS大脑的影响相似。因此，neuropil及其相关元素的减少似乎是TLE的主要特征，而不是继发于细胞损失。在灰质和白质中，神经元肥大意味着更多的核周表面积暴露于突触接触，这是该疾病的标志。
The underlying cause of neocortical involvement in temporal lobe epilepsy (TLE) remains a fundamental and unanswered question. Magnetic resonance imaging has shown a significant loss in temporal lobe volume, and it has been proposed that neocortical circuits are disturbed functionally because neurons are lost. The present study used design-based stereology to estimate the volume and cell number of Brodmann's area 38, a region commonly resected in anterior temporal lobectomy. Studies were conducted on the neocortex of patients with or without hippocampal sclerosis (HS). Results provide the surprising finding that TLE patients have significant atrophy of neocortical gray matter but no loss of neurons. Neurons are also significantly larger, dendritic trees appear sparser, and spine density is noticeably reduced in TLE specimens compared with controls. The increase in neuronal density we found in TLE patients is therefore attributable to large neurons occupying a much smaller volume than in normal brain. Neurons in the underlying white matter are also increased in size but, in contrast to other reports, are not significantly elevated in number or density. Neuronal hypertrophy affects HS and non-HS brains similarly. The reduction in neuropil and its associated elements therefore appears to be a primary feature of TLE, which is not secondary to cell loss. In both gray and white matter, neuronal hypertrophy means more perikaryal surface area is exposed for synaptic contacts and emerges as a hallmark of this disease.