Intranasal administration of rotenone in mice attenuated olfactory functions through the lesion of dopaminergic neurons in the olfactory bulb |
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| Affiliation: | 1. Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD, United States;2. Molecular and Cellular Biology Graduate School Program, Uniformed Services University of the Health Sciences, Bethesda, MD, United States;3. Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences, Bethesda, MD, United States;4. Department of Medical and Clinical Psychology, Uniformed Services University of the Health Sciences, Bethesda, MD, United States;5. Pharmacology Branch, Research Division, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, MD, United States;3. Department of Pathology;5. Electron Microscopy Core Facility, Case Western Reserve University, Cleveland, Ohio 44106;4. Departments of Neurosurgery;6. Neurobiology, Shandong University, Jinan 250012, China;1. Medical Biochemistry Department, Faculty of Medicine, Tanta University, Tanta, Egypt;2. Clinical Pharmacology Department, Faculty of Medicine, Menoufia University, Egypt;3. Physiology Department, Faculty of Medicine, Tanta University, Tanta, Egypt |
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| Abstract: | ![]()
Many environmental chemicals are thought to affect brain function. It was reported that chemicals in the nasal cavity directly reach the brain through the connection between olfactory neurons and the olfactory bulb (OB). In this ‘olfactory transport,’ xenobiotics absorbed at the nasal mucosa reach the brain by bypassing some physical barriers and defenses, and thus olfactory transport is suspected to be a vulnerable mechanism of the brain against invasion threats of environmental chemicals. In this study, we focused on the neuronal toxicity of rotenone administered intranasally to mice. The results showed that the mice that were administered rotenone had attenuated olfactory functions. We also found that intranasally administered rotenone induced acute mitochondrial stress at the OB. The repeated administration of rotenone resulted in a decrease in the number of dopaminergic neurons, which are inhibitory interneurons in the OB. Taken together, our findings suggest that the inhalation of environmental toxins induces the neurodegeneration of cranial neurons through olfactory transport, and that olfactory dysfunction may be induced as an earliest symptom of neurodegeneration caused by inhaled neurotoxins. |
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| Keywords: | Dopaminergic neurons Intranasal administration Mitochondrial stress Olfactory bulb Olfactory transport Rotenone |
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