Ando M, Kunii S, Tatematsu T, Nagata Y
Department of Physiology, Fujita Health University School of Medicine, Aichi, Japan.
Neurosci Res. 1993 Jun;17(1):47-52. doi: 10.1016/0168-0102(93)90028-o.
The activity of transglutaminase (TG), a Ca(2+)-dependent enzyme contributing to cross-linkage formation of intracellular polypeptide chains decreased rapidly to ca. 25% of control level in superior cervical ganglia (SCG) within 0.5 h following denervation. The reduced level was maintained for at least 24 h. By contrast, following axotomy, ganglionic TG activity increased by ca. 50% within 1 h, maintained the increase to 4 h, and returned to control level by 24 h. When SCG were transferred to aerobic in vitro incubation conditions 3 h following denervation, the addition of the protein kinase C (PKC) inhibitor, trifluoperazine (TFP, 10 micrograms/ml), to the medium partially reversed the denervation-induced reduction in ganglionic TG activity. Addition of a PKC activator, 12-O-tetradecanoylphorbol 13-acetate (TPA, 1 microM), had no effect on the TG activity. These findings suggest that the pathway resulting in the rapid, denervation-induced inhibition of TG activity may involve the transsynaptic activation of PKC. When SCG were placed in vitro 3 h following axotomy, addition of nerve growth factor (NGF, 0.25 micrograms/ml) to the medium reversed approximately one-half of the axotomy-induced increase in TG activity. Thus, following axotomy, the reduction in delivery to the SCG of NGF, which can be transported retrogradely within the axon and is indispensable for morphological and functional survival of sympathetic neurons, may trigger the transient, axotomy-induced TG activation in the SCG.
转谷氨酰胺酶(TG)是一种依赖钙离子的酶,有助于细胞内多肽链的交联形成。去神经支配后0.5小时内,颈上神经节(SCG)中该酶的活性迅速降至对照水平的约25%。降低的水平至少维持24小时。相比之下,轴突切断后,神经节TG活性在1小时内增加约50%,在4小时内保持增加状态,并在24小时时恢复到对照水平。去神经支配3小时后,将SCG转移至有氧体外培养条件下,向培养基中添加蛋白激酶C(PKC)抑制剂三氟拉嗪(TFP,10微克/毫升)可部分逆转去神经支配诱导的神经节TG活性降低。添加PKC激活剂12 - O - 十四烷酰佛波醇13 - 乙酸酯(TPA,1微摩尔)对TG活性无影响。这些发现表明,导致去神经支配诱导的TG活性快速抑制的途径可能涉及PKC的跨突触激活。轴突切断3小时后将SCG置于体外,向培养基中添加神经生长因子(NGF,0.25微克/毫升)可逆转约一半的轴突切断诱导的TG活性增加。因此,轴突切断后,NGF向SCG的输送减少(NGF可在轴突内逆行运输,对交感神经元的形态和功能存活不可或缺)可能触发SCG中轴突切断诱导的TG短暂激活。