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Nicotine improved the olfactory impairment in MPTP-Induced Mouse Model of Parkinson's Disease.

08:00 EDT 9th April 2019 | BioPortfolio

Summary of "Nicotine improved the olfactory impairment in MPTP-Induced Mouse Model of Parkinson's Disease."

Olfactory impairment is an early feature of patients with Parkinson's disease (PD). Retrospective epidemiological studies reported lower scores on the University of Pennsylvania Smell Identification Test (UPSIT) in non-smokers than smokers with PD and showed an inverse correlation between susceptibility to PD and a person's history of smoking. But the mechanisms by which cigarettes affect olfaction in PD are not fully understood. So we investigated the effect of nicotine on the olfactory function in 1-methyl-4-phenyl-1, 2, 3, 6 tetrahydropyridine (MPTP)-treated mice. We observed that nicotine improved locomotor activity and protection against dopaminergic neuron loss in the midbrain in MPTP-treated mice. Compared to controls, MPTP-treated mice showed a deficit of odor discrimination and odor detection, which were alleviated by nicotine treatment. But no significant changes were found in olfactory memory in MPTP-treated mice. Moreover, we detected a marked decrease of Choline acetyltransferase (ChAT) expression in the olfactory bulb (OB) in MPTP-treated mice, which was also attenuated by nicotine administration. In addition, nicotine ameliorated the loss of cholinergic neurons and dopaminergic innervation in the horizontal limb of the diagonal band (HDB), which is the primary origin of cholinergic input to the OB. Our results suggested that nicotine could improve the olfactory impairment by protecting cholinergic systems in the OB of MPTP-treated mice. And nicotine protection of cholinergic systems in the OB is relevant to attenuating dopaminergic neuron loss in the midbrain and HDB.

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This article was published in the following journal.

Name: Neurotoxicology
ISSN: 1872-9711
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Medical and Biotech [MESH] Definitions

A condition caused by the neurotoxin MPTP which causes selective destruction of nigrostriatal dopaminergic neurons. Clinical features include irreversible parkinsonian signs including rigidity and bradykinesia (PARKINSON DISEASE, SECONDARY). MPTP toxicity is also used as an animal model for the study of PARKINSON DISEASE. (Adams et al., Principles of Neurology, 6th ed, p1072; Neurology 1986 Feb;36(2):250-8)

Set of nerve fibers conducting impulses from olfactory receptors to the cerebral cortex. It includes the OLFACTORY NERVE; OLFACTORY BULB; olfactory tract, olfactory tubercle, anterior perforated substance, and olfactory cortex. The term rhinencephalon is restricted to structures in the CNS receiving fibers from the olfactory bulb.

Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke.

The 1st cranial nerve. The olfactory nerve conveys the sense of smell. It is formed by the axons of OLFACTORY RECEPTOR NEURONS which project from the olfactory epithelium (in the nasal epithelium) to the OLFACTORY BULB.

One of the first INBRED MOUSE STRAINS to be sequenced. This strain is commonly used as genetic background for transgenic mouse models. Refractory to many tumors, this strain is also preferred model for studying role of genetic variations in development of diseases.

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