Friedman B, Price J L
J Comp Neurol. 1986 Apr 1;246(1):20-31. doi: 10.1002/cne.902460103.
Adult olfactory cortical neurons in layer IIa undergo fulminant transneuronal degeneration after removal of afferent olfactory bulb fibers (Price, '76, Neurosci Abst. 2:161; Heimer and Kalil, '78, J. Comp. Neurol. 178:559-609). This provides an unusual example of dependence of a mature population of neurons on axonal input. In order to investigate whether similar transneuronal degeneration occurs in immature animals, a series of rats were subjected to unilateral olfactory bulb removal at various ages during the first 3 postnatal weeks. The brains were examined for degeneration after short survivals by use of the de Olmos cupric silver method, which selectively stains degenerating neurons. In addition, animals with long survivals were examined with the HRP retrograde tracing method, in order to determine if cells that survive the acute effects of deafferentation develop normal patterns of connections. Young neurons are more resistant to the effects of olfactory bulb removal than more mature neurons. There was little degeneration of cortical neurons after bulb ablation during the first 2 postnatal weeks. Although layer IIa does not become distinct from layer IIb in these experimental animals, cells that have connections normally characteristic of the cells of layer IIa, and are situated at the superficial edge of layer II, were identified with the HRP method. The severity of transneuronal degeneration increases and becomes adultlike between the second and third postnatal weeks. This increase in transneuronal degeneration is temporally associated with a progressive reduction in axonal sprouting following deafferentation during the first 3 postnatal weeks, as described in the companion paper (Friedman and Price, '86). Thus, axon sprouting may "protect" the immature IIa neurons from the effects of removal of the fibers from the olfactory bulb. A period of normal cell death has also been identified in olfactory cortex by the use of the de Olmos cupric silver method. This cellular degeneration is much less severe and has a different time course and laminar distribution than the transneuronal degeneration produced by olfactory bulb ablation in adults. Although normal cell death appears to be potentiated by removal of the olfactory bulb on postnatal day 1, it is clearly a different process from the transneuronal reaction.
在切除传入嗅球纤维后，成年大鼠嗅皮质IIa层的神经元会发生暴发性跨神经元变性（普赖斯，1976年，《神经科学文摘》2:161；海默和卡利尔，1978年，《比较神经学杂志》178:559 - 609）。这提供了一个成熟神经元群体对轴突输入依赖性的不寻常例子。为了研究在未成熟动物中是否发生类似的跨神经元变性，一系列大鼠在出生后的前三周内的不同年龄接受了单侧嗅球切除。通过使用德奥尔莫斯铜银法对短期存活的动物大脑进行检查，该方法可选择性地标记变性神经元。此外，对长期存活的动物采用辣根过氧化物酶逆行追踪法进行检查，以确定在去传入神经的急性影响下存活的细胞是否形成正常的连接模式。年轻神经元比成熟神经元对嗅球切除的影响更具抵抗力。在出生后的前两周内，嗅球切除后皮质神经元几乎没有变性。尽管在这些实验动物中IIa层与IIb层没有明显区分，但通过辣根过氧化物酶法鉴定出了具有IIa层细胞正常特征性连接且位于II层浅边缘的细胞。跨神经元变性的严重程度在出生后第二周和第三周之间增加并变得类似成年状态。如配套论文（弗里德曼和普赖斯，1986年）所述，这种跨神经元变性的增加在时间上与出生后前三周去传入神经后轴突发芽的逐渐减少相关。因此，轴突发芽可能“保护”未成熟的IIa神经元免受嗅球纤维切除的影响。通过使用德奥尔莫斯铜银法，还在嗅皮质中确定了一段正常细胞死亡期。这种细胞变性比成年动物嗅球切除所产生的跨神经元变性要轻得多，并且具有不同的时间进程和层状分布。尽管在出生后第1天切除嗅球似乎会增强正常细胞死亡，但它显然是一个与跨神经元反应不同的过程。
