TRANSNEURONAL DEGENERATION IN THE MIDBRAIN CENTRAL GRAY FOLLOWING CHEMICAL LESIONS IN THE VENTROMEDIAL NUCLEUS - A QUALITATIVE AND QUANTITATIVE-ANALYSIS
TRANSNEURONAL DEGENERATION IN THE MIDBRAIN CENTRAL GRAY FOLLOWING CHEMICAL LESIONS IN THE VENTROMEDIAL NUCLEUS - A QUALITATIVE AND QUANTITATIVE-ANALYSIS
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DOI：
10.1016/0306-4522(90)90038-6
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发表时间：
1990-01-01
期刊：
影响因子：
3.3
通讯作者：
PFAFF, DW
中科院分区：
文献类型：
--
作者：
CHUNG, SK;COHEN, RS;PFAFF, DW
在之前的下丘脑腹内侧核电解损伤实验中，我们显示了大鼠中脑中央灰质的突触前和突触后变性。所看到的突触后变性可能表明腹内侧核对中脑中央灰质的跨神经元效应。然而，电解损伤会破坏传入末梢和通道中的纤维，因此中脑中央灰质中所见的突触后变性可能是由于中脑中央灰质传入神经向腹内侧核的逆行变性或通道中纤维的变性所致。为了区分这些可能性，在腹内侧核中进行化学损伤，即红藻氨酸和N-甲基天冬氨酸，并在损伤后的不同时间间隔检查中脑中央灰色和大脑皮层的超微结构。这两种兴奋毒素已被证明可以破坏神经元，不伤害传入神经末梢和通道中的纤维。在右腹内侧核中接受红藻氨酸损伤的动物允许存活1周，并且在右腹内侧核中接受N-甲基天冬氨酸损伤的动物允许存活4、8和20天。未损伤动物的中脑中央灰色组织作为红藻氨酸和 N-甲基天冬氨酸损伤的对照。此外，其他对照动物的右顶叶皮层注射了等量的N-甲基天冬氨酸，并被允许存活四天和八天。对于上述每种注射和存活条件，将左皮质和中脑中央灰质的细分部分去除并进行电子显微镜处理。接受红藻氨酸和 N-甲基天冬氨酸腹内侧下丘脑损伤的动物显示出突触前和突触后变性的迹象。对腹内侧核和皮质中接受N-甲基天冬氨酸损伤的动物的皮质和中脑中央灰质进行变性的定量分析（一般线性模型程序），并测量了几个参数。接受腹内侧下丘脑损伤并存活8天和20天的动物显示，中脑中央灰质中的退化突触前成分与总突触前成分、退化突触后成分与总突触后成分以及退化总成分与总成分的比率显着高于皮质。 此外，退化的突触后元件与总突触后元件的比率大于其他比率。因此，选择性破坏腹内侧核神经元的效果导致中脑中央灰质的特异性变性，但在8天和20天后，皮层却没有变性。因此，下丘脑腹内侧损伤后中脑灰质中央部出现的突触后变性是由于跨神经元变性，而不是中脑灰质中央部传入神经的逆行变性。这些结果表明，投射到中脑中央灰质的腹内侧核神经元可能对于维持该区域一些神经元的完整性很重要。
In the preceding experiments with electrolytic lesions of the ventromedial nucleus of the hypothalamus, we showed pre- and postsynaptic degeneration in te midbrain central gray of the rat. The postsynaptic degeneration seen may indicate a transneuronal effect of the ventromedial nucleus on the midbrain central gray. Electrolytic lesions, however, destroy afferent endings and fibers in passage, so that the postsynaptic degeneration seen in the midbrain central gray may be due to retrograde degeneration of midbrain central gray afferents to the ventromedial nucleus or due to degeneration of fibers in passage. In order to distinguish among these possibilities, chemical, i.e. kainic acid and N-methyl aspartate, lesions were made in the ventromedial nucleus and the ultrastructure of the midbrain central gray and cerebral cortex was examined at various intervals following the lesions. Both of these excitotoxins have been shown to destroy neurons, sparing afferent terminals and fibers in passage. Animals receiving kainic acid lesions in the right ventromedial nucleus were allowed to survive for one week, and animals receiving N-methyl aspartate lesions in the right ventromedial nucleus were permitted to survive for four, eight, and 20 days. Midbrain central gray tissue of unlesioned animals served as a control for both kainic acid and N-methyl aspartate lesions. In addition, other control animals received injections of the same amount of N-methyl aspartate in the right parietal cortex and were permitted to survive for four and eight days. For each of the above injection and survival conditions, the left cortex and subdivisions of the midbrain central gray were removed and processed for electron microscopy. Animals receiving ventromedial hypothalamic lesions with both kainic acid and N-methyl aspartate showed signs of pre- and postsynaptic degeneration. A quantitative analysis (General Linear Model Procedure) of degeneration was performed on the cortex and midbrain central gray of animals receiving N-methyl aspartate lesions in the ventromedial nucleus and cortex, and several parameters were measured. Animals receiving ventromedial hypothalamic lesions and surviving for eight and 20 days show significantly higher ratios of degenerating presynaptic elements to total presynaptic elements, degenerating postsynaptic elements to total postsynaptic elements, and degenerating total elements to total elements, in the midbrain central gray than in the cortex. Furthermore, the ratio of degenerating postsynaptic elements to total postsynaptic elements is larger than the other ratios. The effect of the selective destruction of ventromedial nucleus neurons, therefore, resulted in specific degeneration in the midbrain central gray but not in the cortex after eight and 20 days. The postsynaptic degeneration seen in the midbrain central gray after ventromedial hypothalamic lesions is due, therefore, to transneuronal degeneration, rather than retrograde degeneration of midbrain central gray afferents. These results suggest that ventromedial nucleus neurons which project to the midbrain central gray may be important in maintaining the integrity of some neurons in that region.