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Differential Regional Responses in Soluble Monomeric Alpha Synuclein Abundance Following Traumatic Brain Injury
S W Carlson1, H Q Yan1, Y Li1
1Neurological Surgery, University of Pittsburgh, 4401 Penn Avenue, Pittsburgh, PA, 15224, USA.
Molecular Neurobiology
|September 19, 2020
Summary
Traumatic brain injury (TBI) reduces monomeric alpha synuclein (α-synuclein) levels in rat brains, particularly the hippocampus, for an extended period. This deficit may impair long-term neurotransmission after TBI.
Area of Science:
- Neuroscience
- Neurobiology
- Cellular Biology
Background:
- Alpha synuclein (α-synuclein) is a neuronal protein primarily located in presynaptic terminals.
- While α-synuclein aggregates are studied in neurodegeneration, monomeric α-synuclein's physiological role and changes post-injury are less understood.
- Evidence suggests α-synuclein plays a role in neurotransmission.
Purpose of the Study:
- To investigate chronic changes in regional monomeric α-synuclein abundance after traumatic brain injury (TBI).
- To assess the impact of TBI on α-synuclein levels in the cortex, hippocampus, and striatum over time.
Main Methods:
- Adult rats underwent controlled cortical impact (CCI) TBI.
- α-synuclein levels were measured using Western blot and immunohistochemistry at various time points (6 hours to 8 weeks post-injury).
- Levels were compared between injured (ipsilateral) and sham animals.
Main Results:
- Monomeric α-synuclein protein levels were significantly decreased in the ipsilateral hippocampus at multiple time points post-TBI.
- Reduced α-synuclein was also observed in the ipsilateral cortex and striatum at specific early time points.
- Immunohistochemistry showed lower α-synuclein and synaptophysin staining in the hippocampus 1 week post-TBI, without aggregate formation.
Conclusions:
- Monomeric α-synuclein abundance is chronically reduced in the hippocampus following TBI.
- This sustained deficit in monomeric α-synuclein may contribute to impaired neurotransmission observed long-term after TBI.

