Developmental pattern of perineuronal nets in the human prefrontal cortex and their deficit in schizophrenia.
Developmental pattern of perineuronal nets in the human prefrontal cortex and their deficit in schizophrenia.
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DOI：
10.1016/j.biopsych.2013.05.007
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发表时间：
2013-09-15
影响因子：
10.6
通讯作者：
Woo, Tsung-Ung W.
中科院分区：
文献类型：
--
作者：
Mauney, Sarah A.;Athanas, Katina M.;Pantazopoulos, Harry;Shaskan, Noel;Passeri, Eleonora;Berretta, Sabina;Woo, Tsung-Ung W.
神经元束膜网（perineuronalnets，PNNs）是一种细胞外基质结构，包裹着大脑中的许多神经元。它们调节出生后依赖经验的脑回路成熟，并通过稳定突触结构来维持其在成熟大脑中的功能完整性。86例死后人脑被纳入本研究。我们使用紫藤花凝集素组织化学可视化PNNs调查是否PNNs的前额叶皮层（PFC）和初级视觉皮层的密度在精神分裂症或双相情感障碍的受试者改变。此外，我们量化的PNNs在人类PFC的正常出生后的发展。与正常对照组相比，PNNs的密度减少了70-76%，在第3层和第5层的PFC精神分裂症，但不是在双相情感障碍。这一发现在另一组精神分裂症患者和正常对照组中得到了证实。此外，初级视觉皮层的PNN密度在两种情况下都没有改变。最后，PFC中的PNN数量在出生后的发育过程中增加，通过围青春期，直到青春期后期和成年早期。这些结果表明，PNN缺陷有助于PFC功能障碍的精神分裂症。事实上，PNN发展的时间与精神分裂症精神病学逐渐出现的时期重叠，提出了异常PNN形成可能有助于疾病发作的可能性。因此，表征PNN缺陷的分子机制可能对精神分裂症的诊断，治疗，早期干预和预防的新策略的概念化具有重要意义。
Perineuronal nets (PNNs) are extracellular matrix structures that enwrap many neurons in the brain. They regulate the postnatal experience-dependent maturation of brain circuits and maintain their functional integrity in the mature brain by stabilizing their synaptic architecture. Eighty-six postmortem human brains were included in this study. We used Wisteria Floribunda agglutinin histochemistry to visualize PNNs to investigate whether the densities of PNNs in the prefrontal cortex (PFC) and primary visual cortex were altered in subjects with schizophrenia or bipolar disorder. In addition, we quantified the normal postnatal development of PNNs in the human PFC. Compared to the normal control subjects, the densities of PNNs were decreased by 70–76% in layers 3 and 5 of the PFC in schizophrenia but not in bipolar disorder. This finding was replicated in a separate group of schizophrenia and normal control subjects. In addition, PNN densities in the primary visual cortex were unaltered in either condition. Finally, the number of PNNs in the PFC increased during postnatal development through the peripubertal period until late adolescence and early adulthood. These findings suggest that PNN deficit contributes to PFC dysfunction in schizophrenia. The fact that the timing of PNN development overlaps with the period when schizophrenia symptomatology gradually emerges raises the possibility that aberrant PNN formation may contribute to the onset of illness. Thus, characterization of the molecular mechanisms underlying PNN deficit may have important implications for the conceptualization of novel strategies for the diagnosis, treatment, early intervention and prevention of schizophrenia.
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影响因子：
4.4
作者：
Bitanihirwe, B. K. Y.;Lim, M. P.;Woo, T. U. W.
通讯作者：
Woo, T. U. W.
DOI：
10.1073/pnas.0609440103
发表时间：
2006-12-26
影响因子：
11.1
作者：
Cho, R. Y.;Konecky, R. O.;Carter, C. S.
通讯作者：
Carter, C. S.
DOI：
10.1007/978-3-7091-0932-8_7
发表时间：
2012-01-01
期刊：
SYNAPTIC PLASTICITY: DYNAMICS, DEVELOPMENT AND DISEASE
影响因子：
--
作者：
Frischknecht, Renato;Gundelfinger, Eckart D.
通讯作者：
Gundelfinger, Eckart D.
影响因子：
2.8
作者：
Brückner, G;Grosche, J;Schachner, M
通讯作者：
Schachner, M
影响因子：
3.3
作者：
Giamanco, K. A.;Matthews, R. T.
通讯作者：
Matthews, R. T.