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Nicotine Inhalant via E-Cigarette Facilitates Sensorimotor Function Recovery by Upregulating Neuronal BDNF-TrkB Signaling in Traumatic Brain Injury
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  • Dongsheng Wang,
  • xiaojing Li,
  • Tiffany Duong,
  • Wenxi Li,
  • Hongxia Wang,
  • Natalia Kleschevnikova,
  • Hemal H. Patel,
  • Ellen Breen,
  • Susan Powell,
  • Shanshan Wang,
  • Brian Head
Dongsheng Wang
University of California San Diego
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xiaojing Li
University of California San Diego
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Tiffany Duong
University of California San Diego
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Wenxi Li
University of California San Diego
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Hongxia Wang
University of California San Diego
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Natalia Kleschevnikova
University of California San Diego
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Hemal H. Patel
VA San Diego Healthcare System
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Ellen Breen
University of California San Diego
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Susan Powell
University of California San Diego
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Shanshan Wang
University of California San Diego
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Brian Head
University of California San Diego

Corresponding Author:[email protected]

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Abstract

Background and Purpose: Traumatic brain injury (TBI) imposes life-long physical, psychological, and financial burdens on affected individuals. The current study investigated the effects of chronic nicotine exposure via E-cigarette (E-cig) on TBI-associated behavioral and biochemical changes. Experimental Approach: Adult C57/BL6J male mice were subjected to controlled cortical impact (CCI) followed by daily exposure to E-cigarette (E-Cig) vapor for six weeks. The effects of chronic nicotine exposure on sensorimotor functions, locomotion, and sociability were evaluated by nesting, open field, and social approach, respectively. Immunoblots were performed to assess changes of mature brain-derived neurotrophic factor (mBDNF) and associated downstream signaling proteins (p-Akt and p-Erk). Histological analyses of the cortex were performed to evaluate the effects of chronic nicotine exposure on Microglia-mediated neuroinflammation. Key Results: Post-injury chronic nicotine exposure significantly improved nesting performance in CCI mice. Histology analysis revealed that chronic nicotine exposure increased the survival of cortical neurons in the perilesion cortex. Immunoblots of cortical tissue revealed that chronic nicotine exposure significantly upregulated mBDNF expression, P-Erk, and p-Akt in the perilesion cortical tissue of CCI mice. Additional IF microscopy revealed elevated mBDNF and p-Akt expression was predominantly localized in cortical neurons of CCI mice. Furthermore, immunolabeling of Iba1 showed that chronic nicotine exposure attenuates microglia-mediated chronic neuroinflammation in the perilesional cortex of CCI mice. Conclusions and Implications: Post-injury chronic nicotine exposure via vaping facilitates sensorimotor function recovery by upregulating neuroprotective mBDNF/TrkB/Akt/Erk signaling. Results from this study support the neuroprotective properties of nicotine, further investigation is needed due to its highly addictive nature.
23 Oct 2023Submitted to British Journal of Pharmacology
24 Oct 2023Assigned to Editor
24 Oct 2023Submission Checks Completed
24 Oct 2023Review(s) Completed, Editorial Evaluation Pending
03 Nov 2023Reviewer(s) Assigned