首页> 外文期刊>Behavioural Brain Research: An International Journal >Re-evaluation of the spatial memory deficits induced by hippocampal short lasting inactivation reveals the need for cortical co-operation.
【24h】

Re-evaluation of the spatial memory deficits induced by hippocampal short lasting inactivation reveals the need for cortical co-operation.

机译:对由海马短暂失活引起的空间记忆缺陷的重新评估揭示了皮质合作的必要性。

获取原文
获取原文并翻译 | 示例
           

摘要

Evidence has accumulated that the rat hippocampus plays a central role in spatial memory. In complement to lesion studies, reversible lidocaine-induced inactivations have been used to investigate the time-course of the memory processes mediated by the hippocampus. A number of studies suggest that, in some conditions, the hippocampus is not necessary for online acquisition of spatial information. To test this hypothesis, we examined the effects of bilateral lidocaine-induced inactivations of the dorsal hippocampus in the acquisition of new spatial information. After initial learning of a place navigation task in the water maze, rats were tested for acquisition of a new platform location and received injections of lidocaine in the hippocampus prior to each daily four-trial block. The training blocks were separated by a 24-h period allowing the hippocampus to recover from inactivation. The results show that lidocaine-injected rats were able to learn the new platform location like controls. Inactivations, however, was found to induce a within-block learning impairment. This suggests that the hippocampus can perform off-line processing and that another structure is able to handle spatial information during hippocampal inactivations. Parietal-lesioned rats that received an injection of lidocaine were still able to learn the new platform location suggesting that the parietal cortex does not sustain this role. Overall, our results suggest that the hippocampus is not necessary for all stages of memory formation and co-operates with other brain, possibly cortical, structures which remain to be determined.
机译:已有证据表明大鼠海马在空间记忆中起着核心作用。作为对病变研究的补充,可逆性利多卡因诱导的失活已用于研究海马介导的记忆过程的时程。大量研究表明,在某些情况下,海马不是在线获取空间信息所必需的。为了验证该假设,我们研究了双边利多卡因诱导的背侧海马失活在获取新的空间信息中的作用。在初步了解水迷宫中的位置导航任务之后,对大鼠进行测试以获取新的平台位置,并在每天进行的四次试验阻止之前,在海马中注射利多卡因。将训练块间隔24小时,以使海马从失活中恢复。结果表明,注射利多卡因的大鼠能够像对照一样学习新的平台位置。然而,发现失活会诱发区块内学习障碍。这表明海马可以执行离线处理,并且另一种结构能够在海马灭活期间处理空间信息。接受利多卡因注射的顶叶病变大鼠仍能够了解新的平台位置,这表明顶叶皮质不能维持这种作用。总的来说,我们的研究结果表明海马并不是记忆形成的所有阶段所必需的,而是与其他大脑,可能还有皮质的结构协同工作,尚待确定。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号