ArticleNeurotrauma reports2025
Assessment of Neurobehavioral Performance and Markers of Synaptic Vesicle Trafficking in an Alpha-Synuclein Knockout Mouse Model after Controlled Cortical Impact Injury.
Article in Neurotrauma reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Traumatic brain injury (TBI) is associated with significant deficits across cognitive, emotional, and somatic functions, contributing to reduced quality of life for TBI survivors. Synaptic vesicle cycling, crucial for neurotransmitter release, involves a tightly regulated process of exocytosis and endocytosis, of which monomeric alpha-synuclein (mAS) is implicated in both, and therefore, may underpin neurotransmission impairments post-TBI. Our team previously demonstrated that controlled cortical impact (CCI) reduces hippocampal and cortical mAS in the weeks postinjury. We hypothesized that genetic knockout (KO) of mAS expression may exacerbate TBI-induced deficits in neurobehavioral performance and synaptic health. To elucidate the role of AS in neurobehavioral recovery and histopathological alterations post-TBI, we employed a genetic AS-KO mouse model (B6;129X1-Snca<tm1Ros1>/J). Markers of exocytosis and endocytosis, cysteine-string protein alpha (CSPα) and clathrin light chain (CLC), respectively, and the astrocytic marker glial fibrillary acidic protein (GFAP) were assessed. Male AS-KO and wild-type (WT) littermate controls received 1.8 mm CCI or Sham control surgery (Sham-WT, CCI-WT, CCI-KO,
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