Sanner C A, Murray M, Goldberger M E
Department of Anatomy and Neurobiology, Medical College of Pennsylvania, Philadelphia 19129.
Exp Neurol. 1993 Sep;123(1):81-90. doi: 10.1006/exnr.1993.1142.
We investigated the effect of axotomy, deafferentation, and deafferentation plus axotomy on cell survival and cell size in Clarke's nucleus of the cat spinal cord. Hemisection of the adult spinal cord at T9 leads to retrograde cell death of 40% of the neurons in Clarke's nucleus at L3, as well as to a reduction in the mean soma size of the survivors. In contrast, deafferentation of Clarke's nucleus neurons by L1-S2 dorsal rhizotomy produces no cell loss and no shrinkage of the somata. These results indicate that dorsal root afferent input is not required for Clarke's nucleus cell survival. To test whether afferents may be required by the 60% of neurons that survive axotomy, we deafferented Clarke's nucleus prior to axotomy. Surprisingly, removal of primary afferents to Clarke's nucleus neurons prior to axotomy prevented the death of all neurons that would normally have died from axotomy. These results suggest that dorsal root afferent input is not required for Clarke's nucleus neuron survival after axotomy and may in fact be toxic to these axotomized neurons. This afferent toxicity is likely to be mediated through the dorsal root afferent neurotransmitter glutamate.
我们研究了轴突切断、传入神经阻滞以及传入神经阻滞加轴突切断对猫脊髓克拉克核中细胞存活和细胞大小的影响。在T9水平对成年猫脊髓进行半横断，会导致L3水平克拉克核中40%的神经元发生逆行性细胞死亡，同时存活神经元的平均胞体大小也会减小。相比之下，通过L1 - S2背根切断术对克拉克核神经元进行传入神经阻滞，不会导致细胞丢失，胞体也不会缩小。这些结果表明，克拉克核细胞存活不需要背根传入神经输入。为了测试轴突切断后存活的60%的神经元是否需要传入神经，我们在轴突切断之前对克拉克核进行了传入神经阻滞。令人惊讶的是，在轴突切断之前去除克拉克核神经元的初级传入神经，可防止所有正常情况下会因轴突切断而死亡的神经元死亡。这些结果表明，轴突切断后克拉克核神经元存活不需要背根传入神经输入，实际上传入神经对这些轴突切断的神经元可能有毒性。这种传入神经毒性可能是通过背根传入神经递质谷氨酸介导的。
