通过损伤CA1锥体细胞兴奋性传入神经，可以预防破伤风毒素对大鼠造成的海马损伤。

Hippocampal damage produced by tetanus toxin in rats can be prevented by lesioning CA1 pyramidal cell excitatory afferents.

作者信息

Bagetta G, Nisticó G, Bowery N G

机构信息

Department of Pharmacology, School of Pharmacy, London, U.K.

出版信息

Neurosci Lett. 1991 Feb 11;123(1):32-6. doi: 10.1016/0304-3940(91)90151-i.

DOI:10.1016/0304-3940(91)90151-i

PMID:2062452

Abstract

The neuropathological effects induced by tetanus toxin (TT) bilaterally microinjected into the hippocampus were studied in rats bearing a surgical unilateral lesion of the Schaffer collaterals. TT (1000 mouse minimum lethal doses, MLDs; n = 5 rats) produced neurodegeneration in the CA1 pyramidal cell layer in the unlesioned side of the hippocampus ten days after injection. By contrast, the injection of TT into the lesioned hippocampus produced no degeneration. In rats bilaterally treated with BSA (n = 3 rats) no neuropathological effects were observed in either hippocampi. In conclusion, our results have demonstrated that the lesion of the Schaffer collaterals may protect against the neuropathological effects induced by TT in rats.

摘要

在一侧海马体的Schaffer侧支遭受手术损伤的大鼠中，研究了双侧海马体微量注射破伤风毒素（TT）所诱导的神经病理学效应。注射TT（1000个小鼠最小致死剂量，MLDs；n = 5只大鼠）后十天，在海马体未损伤侧的CA1锥体细胞层产生了神经退行性变。相比之下，向损伤的海马体注射TT未产生退变。在用牛血清白蛋白双侧处理的大鼠（n = 3只大鼠）中，两侧海马体均未观察到神经病理学效应。总之，我们的结果表明，Schaffer侧支的损伤可能对TT在大鼠中诱导的神经病理学效应具有保护作用。