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Related Experiment Video

Updated: Jun 5, 2026

Live Imaging of Nicotine Induced Calcium Signaling and Neurotransmitter Release Along Ventral Hippocampal Axons

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Published on: June 24, 2015

Nicotine aggravates the brain postischemic inflammatory response.

Shayna T Bradford¹, Svetlana M Stamatovic, Raj S Dondeti

¹Department of Pathology, University of Michigan, Medical School, Ann Arbor, 48109-0532, USA.

American Journal of Physiology. Heart and Circulatory Physiology

|January 18, 2011

Summary

Nicotine exposure increases inflammatory responses in brain endothelial cells, worsening stroke outcomes. This study reveals how nicotine impacts the brain

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Probing Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices via Laser Flash Photolysis of Photoactivatable Nicotine

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Published on: January 25, 2019

Area of Science:

Neuroscience
Vascular Biology
Toxicology

Background:

Nicotine is a known risk factor for stroke, affecting cerebral blood flow and the blood-brain barrier.
Existing evidence suggests nicotine's detrimental impact on cerebrovascular health.

Purpose of the Study:

To investigate the effects of nicotine on cerebrovascular endothelium.
To examine nicotine's role in basal and ischemia/reperfusion (I/R) injury in vivo.

Main Methods:

Mice were administered nicotine (2 mg/kg sc) for 14 days, achieving plasma levels similar to heavy smokers.
Brain microvessels were analyzed for phenotypic changes, including inflammatory mediator expression.
Leukocyte infiltration and ischemia/reperfusion injury markers (infarct size, neurological deficits, mortality) were assessed.

Main Results:

Nicotine exposure elevated inflammatory mediators (cytokines, chemokines) and adhesion molecules in brain microvessels.
This was associated with increased leukocyte infiltration during ischemia/reperfusion.
Nicotine significantly exacerbated ischemia/reperfusion injury, leading to larger infarcts, worse neurological deficits, and higher mortality.

Conclusions:

Nicotine alters brain endothelial cell phenotype, promoting inflammation.
Nicotine exacerbates the inflammatory response to ischemia/reperfusion injury in the brain.
These findings elucidate nicotine's mechanism in regulating the brain-vascular interface during ischemic events.