Changes in microtubule-associated protein 2 and amyloid precursor protein immunoreactivity following traumatic brain injury in rat: influence of MK-801 treatment
Abstract
We investigated by immunohistochemistry dendritic and axonal changes occurring in the rat brain after mild focal cortical trauma produced by the weight drop technique. One and 3 days after injury, nerve cell bodies and dendrites in the perimeter of the impact site displayed decreased microtubule-associated protein 2 (MAP2) immunoreactivity. Some dendrites in the immediate adjacent region were more intensely stained and distorted. The dentate hilar region of the hippocampus showed a reduction of immunoreactive nerve cell bodies and dendrites. Twenty-one days after injury the strongly stained cortical dendrites and the reduction of immunoreactivity in the hippocampus remained, whereas the reduced staining in the perimeter of the lesion had normalised. These results indicate that there is a long-lasting disturbed dendritic organisation implicating impaired neurotransmission after this type of mild brain trauma. beta-Amyloid precursor protein (APP) immunohistochemistry revealed numerous stained axons in the ipsilateral subcortical white matter and thalamus indicating local and remote axonal injuries with disturbed axonal transport. Twenty-one days after injury, numerous small immunostained profiles appeared in the neuropil of the cortical impact site and in the ipsilateral thalamus. The axonal changes indicate disturbed connectivity between the site of the impact and other brain regions, chiefly the thalamus. The presence of beta-amyloid was investigated 21 days after trauma. The…
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A majority of rodent studies fail to show Aβ deposition after TBI in non-transgenic animals using CCI, FPI, and weight drop models.
“a majority of rodent studies fail to show this association in non-transgenic animals using CCI, FPI, and weight drop models (121, 122, 124, 125, 135).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [135]
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References 49 · Cited by 90
- Authors
- Lewén, A., Li, G. L., Olsson, Y., & Hillered, L.
- Affiliations
- Uppsala University Hospital (SE)
- Corresponding author
- Lewén, Anders
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 1996-05
- Volume
- 719
- Issue
- 1-2
- Pages
- 161-171
- ISSN
- 0006-8993 (ISSN-L)
- OpenAlex
- W1985722784
- Cited by
- 90
- References
- 49
- Citations by year
- 2022: 1 · 2018: 3 · 2017: 2 · 2016: 1 · 2014: 1 · 2013: 3 · 2012: 5
- FWCI
- 4.57
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Automotive and Human Injury Biomechanics
- Keywords
- traumatic brain injury, MAP2, amyloid precursor protein, MK-801, NMDA receptor antagonism, dendritic changes, axonal injury, axonal transport, hippocampus, thalamus, white matter, amyloid-beta, neurotoxicity, weight-drop injury
- MeSH terms
- Animals, Brain Injuries, Immunohistochemistry, Male, Microtubule-Associated Proteins, Nerve Tissue Proteins, Receptors, N-Methyl-D-Aspartate, Dizocilpine Maleate, Amyloid beta-Protein Precursor, Rats, Sprague-Dawley, Excitatory Amino Acid Antagonists, Neuroprotective Agents, Rats
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