The Effect of Postinjury Kindled Seizures on Cognitive Performance of Traumatically Brain-Injured Rats

The purpose of this experiment was to examine the consequences of postinjury seizures on cognitive performance after experimental traumatic brain injury (TBI). Rats either were injured at a moderate (2.1 atm) level of central fluid percussion TBI ( n = 16) or were surgically prepared but did not rec...

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Bibliographic Details
Published inExperimental neurology Vol. 136; no. 2; pp. 143 - 148
Main Authors Hamm, Robert J., Pike, Brian R., Temple, Meredith D., O'Dell, Dianne M., Lyeth, Bruce G.
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier Inc 01.12.1995
Elsevier
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Summary:The purpose of this experiment was to examine the consequences of postinjury seizures on cognitive performance after experimental traumatic brain injury (TBI). Rats either were injured at a moderate (2.1 atm) level of central fluid percussion TBI ( n = 16) or were surgically prepared but did not receive a fluid pulse (sham-injured control, n = 16). Beginning 24 h after TBI, injured animals were injected (ip) once daily (Days 1-24 postinjury) with either saline ( n = 8) or 25 mg/kg pentylenetetrazol (PTZ) ( n = 8). Sham-injured rats were injected with an equal volume of saline ( n = 8) or PTZ ( n = 8). In both injured and sham-injured animals, daily injections of PTZ resulted in an increase in the severity of behavioral seizures over days. On Days 25-29 after injury or sham injury, all animals were tested in the Morris water maze (MWM). Analysis of maze performance indicated that in sham-injured animals PTZ-produced seizures had a detrimental effect on performance. In injured animals, however, PTZ-treated animals exhibited significantly faster acquisition and better terminal performance in the MWM than did untreated injured animals. These results show that posttraumatic kindled seizures do not exacerbate behavioral deficits after TBI and may, in fact, improve recovery following injury. The findings of this experiment are consistent with the hypothesis that post-TBI neuronal depression may contribute to behavioral morbidity following injury.
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ISSN:0014-4886
1090-2430
DOI:10.1006/exnr.1995.1091