Related Experiment Video
Updated: Jan 6, 2026

15:04
Modeling and Simulations of Olfactory Drug Delivery with Passive and Active Controls of Nasally Inhaled Pharmaceutical Aerosols
Published on: May 20, 2016
11.3K
Characterization of an olfactory system dysfunction model: a vanadium dose-effect study via nose-to-brain delivery in
Margarida Pereira1,2, Carlos Venâncio1,2, Maria Lurdes Pinto3
1Department of Animal Sciences, School of Agrarian and Veterinary Sciences, University of Trás-os-Montes and Alto Douro (UTAD), Vila Real, Portugal.
Frontiers in Neuroanatomy
|October 8, 2025
Summary
Vanadium pentoxide delivered nose-to-brain caused olfactory deficits and neurotoxicity in rats. This animal model is useful for studying neurodegenerative diseases and olfactory dysfunction.
Area of Science:
- Neuroscience
- Toxicology
Background:
- The olfactory system provides a direct neural link to the brain, making it susceptible to xenobiotics and a model for neurotoxicity.
- Studying olfactory dysfunction is crucial for understanding neurodegenerative effects.
Purpose of the Study:
- To characterize an animal model of olfactory dysfunction induced by nose-to-brain (NTB) delivery of vanadium pentoxide (V2O5).
Main Methods:
- Rats received V2O5 intranasally over 4 weeks.
- Analyses included behavioral, histological, and biochemical assessments of the olfactory epithelium (OE), olfactory bulbs (OBs), and hippocampus.
Main Results:
- V2O5 exposure caused olfactory deficits, OE necrosis, OB glomerular changes, and hippocampal neuronal loss.
- Neuroinflammation and oxidative stress markers showed dose-dependent increases in the OBs and hippocampus.
- Proliferating cell nuclear antigen (PCNA) and glial markers indicated cellular proliferation and damage.
Conclusions:
- Nose-to-brain V2O5 delivery induces dose-dependent neurotoxicity, impacting olfactory and cognitive functions.
- This model effectively mimics olfactory dysfunction and neurodegeneration.
- It serves as a valuable tool for investigating mechanisms of olfactory dysfunction and neurodegeneration.

