Evaluation of Memory Dysfunction Following Experimental Brain Injury Using the Morris Water Maze

被引:306
作者
Smith, Douglas H. [1 ]
Okiyama, Koichi [1 ]
Thomas, Mark J. [1 ]
Claussen, Brian [1 ]
McIntosh, Tracey K. [1 ]
机构
[1] Univ Connecticut, CNS Injury Lab, Surg Res Ctr, Dept Surg,Hlth Ctr, Farmington, CT 06030 USA
关键词
D O I
10.1089/neu.1991.8.259
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Memory dysfunction, a common clinical feature of traumatic brain injury (TBI), is thought to be related to secondary damage of key anatomic structures in the brain, including the hippocampus. In the present study, we have characterized and evaluated a novel experimental paradigm using the Morris water maze (MWM) technique, to measure post-TBI memory retention after lateral (parasagittal) fluid percussion (FP) brain injury in rats. Male Sprague-Dawley rats (n = 37) received a total of 20 training trials over 2 days in the MWM. Two and a half hours after the last training trial, the animals received FP brain injury of moderate severity (2.3 atmospheres, n = 12), high severity (2.6 atm, n = 13), or no injury (n = 12). Forty-two hours after FP brain injury, we observed a highly sufficient memory dysfunction in animals from both injury groups compared to the uninjured group (p < 0.001). The degree of memory dysfunction was found to be directly related to the severity of injury, with the high severity group scoring significantly worse than the moderately injured group (p = 0.15). In addition, hippocampal cell loss was observed after brain injury, but only unilaterally. These data suggest that lateral FP brain injury causes memory dysfunction possibly related to concurrent hippocampal cell loss and that posttraumatic memory deficits may be sensitively quantitated using the memory testing paradigm described.
引用
收藏
页码:259 / 269
页数:11
相关论文
共 40 条
[1]   THE DISTRIBUTION OF HYPOGLYCEMIC BRAIN-DAMAGE [J].
AUER, RN ;
WIELOCH, T ;
OLSSON, Y ;
SIESJO, BK .
ACTA NEUROPATHOLOGICA, 1984, 64 (03) :177-191
[2]   LONG-LASTING POTENTIATION OF SYNAPTIC TRANSMISSION IN DENTATE AREA OF ANESTHETIZED RABBIT FOLLOWING STIMULATION OF PERFORANT PATH [J].
BLISS, TVP ;
LOMO, T .
JOURNAL OF PHYSIOLOGY-LONDON, 1973, 232 (02) :331-356
[3]  
BRIERLEY JB, 1976, GREENFIELDS NEUROPAT, P43
[4]  
CHOI DW, 1987, J NEUROSCI, V7, P357
[5]  
COLLINGRIDGE GL, 1989, NMDA RECEPTOR, P123
[6]   NMDA RECEPTORS - THEIR ROLE IN LONG-TERM POTENTIATION [J].
COLLINGRIDGE, GL ;
BLISS, TVP .
TRENDS IN NEUROSCIENCES, 1987, 10 (07) :288-293
[7]   EXPERIMENTAL FLUID PERCUSSION BRAIN INJURY - VASCULAR DISRUPTION AND NEURONAL AND GLIAL ALTERATIONS [J].
CORTEZ, SC ;
MCINTOSH, TK ;
NOBLE, LJ .
BRAIN RESEARCH, 1989, 482 (02) :271-282
[8]  
DISBREY BD, 1970, HISTOLOGICAL LAB MET, P230
[9]  
FADEN AI, 1989, SCIENCE, V244, P789
[10]  
Halgren E., 1988, NEUROPSYCHOLOGY MEMO, P165