Effects of excess thyroid hormone on cell death, cell proliferation, and new neuron incorporation in the adult zebra finch telencephalon.

Effects of excess thyroid hormone on cell death, cell proliferation, and new neuron incorporation in the adult zebra finch telencephalon.
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过量甲状腺激素对成年斑胸草雀端脑细胞死亡、细胞增殖和新神经元掺入的影响。

DOI:
10.1002/neu.10053
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发表时间:
2002
期刊:
Journal of neurobiology
影响因子:
--
通讯作者:
Kirn,JR
Kirn,JR
中科院分区:
--
文献类型:
--
作者:
Tekumalla,PK;Tontonoz,M;Hesla,MA;Kirn,JR

文献摘要

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Widespread telencephalic neuronal replacement occurs throughout life in birds. We explored the potential relationship between thyroxine (T4) and cell turnover in the adult male zebra finch. We found that many cells in the zebra finch brain, including long‐projection neurons in the high vocal center (HVC), stained positively with an antibody to thyroid hormone receptors (TR). Labeling was generally weak in the ventricular zone (VZ) that gives rise to new neurons but some proliferative VZ cells and/or their progeny, identified by [3H]‐thymidine labeling, co‐labeled with anti‐TR antibody. Acute T4treatment dramatically increased the number of pyknotic and TUNEL‐positive cells in HVC and other telencephalic regions. In contrast, degenerating cells were never observed in the archistriatum or sub‐telencephalic regions, suggesting that excess T4augments cell death selectively in regions that show naturally occurring neuronal turnover. VZ mitotic activity was not altered shortly after acute T4treatment at a dosage that stimulated cell death, although [3H]‐labeling intensity per cell was slightly reduced. Moreover, the incorporation rates for neurons formed shortly before or after acute hormone treatment were no different from control values. Chronic T4treatment resulted in a reduction in the total number of HVC neurons. Thus, hyperthyroidism augmented neuronal death, which was not compensated for by neuronal replacement. Collectively, these results indicate that excess T4affects adult neuronal turnover in birds, and raises the possibility that thyroxine plays an important role in the postnatal development of the avian brain and vocal behavior. © 2002 Wiley Periodicals, Inc. J Neurobiol 51: 323–341, 2002