Delayed, selective neuronal death following experimental cortical impact injury in rats: possible role in memory deficits

Brain Res. 1996 Nov 11;739(1-2):111-9. doi: 10.1016/s0006-8993(96)00819-0.


Clinical and experimental studies show that loss of neurons in the hippocampus and/or the entorhinal cortex can impede formation and storage of spatial memory. Using a controlled cortical impact model of traumatic brain injury (TBI) in rats, we have examined the temporal and spatial pattern of neuronal death using silver impregnation and cresyl violet staining. Dystrophic neurons can be detected in the dentate gyrus, and the CA1 and CA3 subfields of the hippocampus for up to 2 weeks following injury. These dystrophic cells appeared shrunken and possessed features of apoptosis. Areas containing the dystrophic cells suffer substantial cell loss as demonstrated by thinning of the neuronal layers. Dystrophic cells are also found in the amygdala, entorhinal and piriform cortices, thalamic and hypothalamic regions, and surrounding the contusion site. The loss of these cells may contribute to the memory deficits observed following TBI.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Benzoxazines
  • Cerebral Cortex / injuries*
  • Cerebral Cortex / pathology
  • Coloring Agents
  • Dentate Gyrus / pathology
  • Hypothalamus / pathology
  • Limbic System / pathology
  • Male
  • Memory Disorders / pathology*
  • Nerve Degeneration / physiology*
  • Neurons / pathology*
  • Olfactory Bulb / pathology
  • Oxazines
  • Rats
  • Rats, Sprague-Dawley
  • Silver Staining
  • Thalamus / pathology
  • Time Factors


  • Benzoxazines
  • Coloring Agents
  • Oxazines
  • cresyl violet