Chronic intermittent nicotine administration attenuates traumatic brain injury-induced cognitive dysfunction.
Chronic intermittent nicotine administration attenuates traumatic brain injury-induced cognitive dysfunction.
复制标题
慢性间歇性尼古丁给药可减轻创伤性脑损伤引起的认知功能障碍。
DOI：
10.1016/s0306-4522(03)00206-9
复制
发表时间：
2003
期刊：
影响因子：
3.3
通讯作者：
Pauly,JR
中科院分区：
文献类型：
--
作者：
Verbois,SL;Hopkins,DM;Scheff,SW;Pauly,JR
Traumatic brain injury (TBI) initiates immediate and secondary neuropathological cascades that can result in persistent neurological dysfunction. Previous studies from our laboratory have shown that experimental rat brain injury causes a rapid and persistent decrease in CNS α7* nicotinic cholinergic receptor (nAChr) expression. The purpose of this study was to investigate whether intermittent nicotine injections could improve cognitive performance in the Morris water maze (MWM) following experimental brain injury. Adult male rats were anesthetized and subjected to a 1.5 mm controlled cortical impact (CCI) injury of the somatosensory cortex. Animals received twice daily i.p. nicotine injections for 11 days prior to CCI, 11 days following CCI or during both pre- and post-surgical intervals. MWM training was initiated 12 days post-injury. In the training phase of cognitive testing, twice-daily nicotine treatment following injury attenuated trauma-induced deficits in the distance traveled to reach the escape platform. This group of animals also had improvements in several measures of the probe test, including time spent, distance traveled and total entries into the target quadrant. TBI caused significant deficits in α7* nAChr expression in several regions of the hippocampus and cerebral cortex, which were largely unaffected by intermittent nicotine treatment. However, nicotine treatment up-regulated [3H]-epibatidine binding to non-α7* nAChrs, attenuating TBI-induced deficits in receptor expression in several brain regions evaluated. These results suggest that nicotine is efficacious at attenuating CCI-induced cognitive deficits in a manner independent of changes in α7* nAChr expression, perhaps via up-regulation of non-α7* nAChrs.
