Related Experiment Video
Updated: Aug 20, 2026
Minimizing Hypoxia in Hippocampal Slices from Adult and Aging Mice
Published on: July 2, 2020
Effect of hypothermia on postmortem alterations in MAP2 immunostaining in the human hippocampus
Osamu Kitamura1, Takako Gotohda, Akiko Ishigami
1Department of Forensic Medicine, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto, Tokushima 770-8503, Japan. northv@basic.med.tokushima-u.ac.jp
Abstract:
Ischemic neuronal injury induce degradation of microtubule-associated protein 2 (MAP2). In addition to ischemia, postmortem brains show alterations in MAP2 immunoreactivity in the hippocampus, suggesting that the factors inducing cytoskeletal disruption in postmortem brain are similar to those in ischemic brains. Hypothermia reduces the severity of ischemic injury including disruption of MAP2 in the hippocampus. However, whether hypothermia reduces postmortem changes of MAP2 was not clear. In this study, we evaluated the effect of hypothermia on postmortem degradation of MAP2 in the human hippocampus at various postmortem intervals using immunohistochemistry. In postmortem brains without hypothermia (the normothermic group), the locus of MAP2 immunoreactivity moved from the dendrites to the cell bodies prior to becoming undetectable with increasing postmortem interval, particularly in the CA1-subiculum region. On the other hand, the change in MAP2 immunoreactivity was remarkably attenuated in brains of death from cold (the hypothermic group). The present study demonstrated that MAP2 disruption is remarkable in the CA1-subiculum region of autopsied brains and that hypothermia reduces the postmortem change of MAP2, as observed in ischemic brain. Therefore, immunostaining of MAP2 in the hippocampus could be used to diagnose hypothermia.
Insights
Hypothermia protects microtubule-associated protein 2 (MAP2) from postmortem degradation in the human hippocampus. This finding suggests MAP2 immunostaining can help diagnose hypothermia, similar to its role in assessing ischemic brain injury.
Area of Science:
- Neuroscience
- Forensic Pathology
- Cell Biology
Background:
- Ischemic neuronal injury causes degradation of microtubule-associated protein 2 (MAP2).
- Postmortem brains exhibit altered MAP2 immunoreactivity, similar to ischemic changes.
- Hypothermia mitigates ischemic injury and MAP2 disruption, but its effect on postmortem MAP2 changes is unknown.
Purpose of the Study:
- To investigate the effect of hypothermia on postmortem MAP2 degradation in the human hippocampus.
- To determine if hypothermia can preserve MAP2 immunoreactivity in postmortem brain tissue.
- To explore the potential of MAP2 immunostaining as a diagnostic marker for hypothermia.
Main Methods:
- Immunohistochemistry was used to evaluate MAP2 immunoreactivity in human hippocampal tissue.
- Samples were analyzed from individuals with varying postmortem intervals.
- Comparison was made between normothermic and hypothermic (death from cold) groups.
Main Results:
- In normothermic brains, MAP2 immunoreactivity shifted from dendrites to cell bodies and became undetectable with increasing postmortem interval, especially in the CA1-subiculum region.
- Hypothermia significantly attenuated postmortem MAP2 degradation.
- MAP2 disruption was pronounced in the CA1-subiculum region of normothermic autopsied brains.
Conclusions:
- Postmortem degradation of MAP2 in the hippocampus, particularly the CA1-subiculum region, is substantial.
- Hypothermia effectively reduces postmortem MAP2 changes, mirroring its protective effects in ischemic brain injury.
- Hippocampal MAP2 immunostaining may serve as a diagnostic indicator for hypothermia.
