Bagetta G, Corasaniti M T, Berliocchi L, Navarra M, Finazzi-Agrò A, Nisticò G
Department of Neuroscience, University of Cagliari, Italy.
Biochem Biophys Res Commun. 1995 Jun 6;211(1):130-6. doi: 10.1006/bbrc.1995.1787.
In the present experiments we have used morphological techniques to study the neuropathological profile of the brain of rats after intracerebroventricular (i.c.v.) injection of recombinant HIV-1 gp 120. Using brain cryostat sections (10 microns) from rats treated with a single, daily dose of gp120 (100 ng/rat) given for 7 and 14 consecutive days, in situ DNA fragmentation was revealed in the neocortex but not in the hippocampus by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end-labelling (TUNEL). In these rats, dark degenerating neurones were observed in the neocortex but not in the hippocampus. Treatment with bovine serum albumin (300 ng/rat, i.c.v.) for up to 14 days did not produce DNA fragmentation nor did it yield neuropathological lesions of the neocortex or hippocampus. In conclusion, the present data demonstrate that gp 120 given i.c.v. produced DNA fragmentation in the neocortex, thus suggesting that apoptosis is the mechanism through which neurones of the neocortex are killed.
在本实验中，我们运用形态学技术研究了脑室内（i.c.v.）注射重组HIV-1 gp120后大鼠脑的神经病理学特征。使用连续7天和14天每天单剂量给予gp120（100 ng/大鼠）处理的大鼠的脑冰冻切片（10微米），通过末端脱氧核苷酸转移酶（TdT）介导的dUTP-生物素缺口末端标记（TUNEL）法，在新皮质中发现了原位DNA片段化，而在海马体中未发现。在这些大鼠中，新皮质中观察到深色变性神经元，而海马体中未观察到。用牛血清白蛋白（300 ng/大鼠，i.c.v.）处理长达14天未产生DNA片段化，也未导致新皮质或海马体出现神经病理学损伤。总之，目前的数据表明，脑室内给予gp120会在新皮质中产生DNA片段化，从而提示凋亡是新皮质神经元被杀死的机制。
