Prins M L, Hovda D A
Department of Neurobiology, Los Angeles, California, USA.
J Neurotrauma. 2001 Jan;18(1):31-46. doi: 10.1089/089771501750055758.
Previous studies have demonstrated that, compared to adults, postnatal day 17 (P17) and P28 rats show remarkable cognitive recovery in the Morris water maze (MWM) following fluid percussion injury (FPI). This observed age-at-trauma effect could result from either younger animals solving the MWM task using noninjured neural circuitry or an inability of adult and P28 brains to activate appropriate neural networks due to trauma-induced neurological dysfunction. To address these possibilities, we compared "activated" brain regions during normal MWM acquisition and following FP injury. To generate "activated" images of the brain while animals were performing the MWM task, qualitative [14C]2-deoxy-D-glucose was conducted on days 2, 5, and 14 during training in sham and injured adult, P28, and P17 rats. When maturational changes in cerebral glucose metabolism are taken into account, the results suggests similar activity changes in the cerebral cortex and lacunosum moleculare of CA1 during acquisition in all age groups, suggesting that the developmental rates of MWM learning do not correspond to different patterns of activated cerebral metabolism. Injured P17s, showing no latency deficits, revealed activated cerebral metabolic patterns similar to noninjured P17 animals. In P28 and adult cases, animals exhibited cognitive deficits and their metabolic studies indicated that the cortical-hippocampal pattern of activation was disrupted by marked injury-induced metabolic depression, which primarily affected the ipsilateral hemisphere and lasted for as long as 14 days in adult animals.
先前的研究表明，与成年大鼠相比，出生后第17天（P17）和P28天的大鼠在液体冲击伤（FPI）后在莫里斯水迷宫（MWM）中表现出显著的认知恢复。这种观察到的创伤时年龄效应可能是由于幼龄动物使用未受损的神经回路解决MWM任务，或者是由于创伤诱导的神经功能障碍，成年和P28天的大脑无法激活适当的神经网络。为了解决这些可能性，我们比较了正常MWM训练期间和FP损伤后的“激活”脑区。为了在动物执行MWM任务时生成大脑的“激活”图像，在假手术组以及成年、P28和P17损伤大鼠训练的第2、5和14天进行了定性[14C]2-脱氧-D-葡萄糖实验。考虑到脑葡萄糖代谢的成熟变化，结果表明在所有年龄组的训练过程中，CA1区的大脑皮层和分子层的活动变化相似，这表明MWM学习的发育速率与激活的脑代谢模式不同无关。未表现出潜伏期缺陷的损伤P17大鼠，其大脑代谢激活模式与未损伤的P17动物相似。在P28和成年大鼠中，动物表现出认知缺陷，它们的代谢研究表明，皮层-海马激活模式被明显的损伤诱导的代谢抑制所破坏，这种抑制主要影响同侧半球，在成年动物中持续长达14天。
