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Olfactory Receptors: Location and Structure

Olfactory Receptors: Location and Structure

The process of olfaction, also known as the sense of smell, is a sophisticated chemical response system. The specialized sensory neurons that facilitate this process, known as olfactory receptor neurons, are situated in an upper segment of the nasal cavity, known as the olfactory epithelium. Olfactory sensory neurons are bipolar, with their dendrites extending from the epithelium's apex into the mucus that lines the nasal cavity. Airborne molecules, when inhaled, traverse the olfactory...

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Updated: Apr 19, 2026

Ex Vivo Preparations of the Intact Vomeronasal Organ and Accessory Olfactory Bulb

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Published on: August 4, 2014

Functional and morphological olfactory bulb modifications in mice after vanadium inhalation.

Laura Colín-Barenque¹, Jose Pedraza-Chaverri², Omar Medina-Campos²

¹Department of Neuroscience, FES Iztacala Edo de México, México. UNAM barenque@unam.mx.

Toxicologic Pathology

|December 11, 2014

Summary

Inhaled vanadium pentoxide (V2O5) exposure in mice impaired olfactory function and caused cellular damage in the olfactory bulb. This suggests vanadium

Keywords:

dendritic spines granule cells olfactory bulb oxidative stress reactive oxygen species vanadium

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Area of Science:

Environmental toxicology
Neuroscience
Cell biology

Background:

Neurodegenerative diseases like Parkinson's and Alzheimer's are linked to impaired olfaction.
Environmental pollutants, including vanadium, are implicated in these pathologies.
Vanadium's toxicity is associated with oxidative stress.

Purpose of the Study:

To investigate the effects of inhaled vanadium pentoxide (V2O5) on olfactory function.
To examine histological and ultrastructural changes in the olfactory bulb granule cells.
To assess the impact on antioxidant enzyme activity in the olfactory bulb.

Main Methods:

Mice inhaled either saline (control) or 0.02-M V2O5 for 4 weeks.
Olfactory function was tested using an odorant test.
Olfactory bulbs were analyzed for antioxidant enzyme activity (GPx, GR), and granule cell morphology via Golgi staining and electron microscopy.

Main Results:

Vanadium exposure significantly decreased olfactory function after 4 weeks.
Granule cells exhibited reduced dendritic spine density, increased lipofuscin, and signs of apoptosis and necrosis.
Activity of glutathione peroxidase (GPx) and glutathione reductase (GR) in the olfactory bulb increased.

Conclusions:

Inhaled vanadium pentoxide disrupts olfactory function and causes cellular damage in the olfactory bulb.
These vanadium-induced changes, potentially mediated by oxidative stress, may serve as a risk factor for neurodegenerative diseases.
The study highlights the neurotoxic potential of environmental vanadium exposure on the olfactory system.