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Social odor recognition: a novel behavioral model for cognitive dysfunction in Parkinson's disease.
Neurodegener Dis. 2010; 7(1-3):153-9.ND

Abstract

BACKGROUND

Parkinson's disease (PD) is a progressive neurodegenerative condition characterized by an increasing loss of dopaminergic neurons resulting in motor dysfunction. However, cognitive impairments in PD patients are a common clinical feature that has gained increased attention.

OBJECTIVE

The purpose of the current study was to evaluate the effects of an MPTP-induced dopaminergic lesion in mice on social odor recognition (SOR) memory.

METHODS

Mice were acutely treated with MPTP and evaluated for memory impairments in the SOR assay and characterized using biochemical and immunohistochemical methods approximately 2 weeks later.

RESULTS

Here we demonstrate that SOR memory is sensitive to MPTP treatment and that it correlates with multiple measures of nigrostriatal integrity. MPTP treatment of C57BL/6N mice produced a profound decrease in dopamine levels, dopamine transporter binding and tyrosine hydroxylase immunoreactivity in the striatum. These impairments in stratial dopaminergic function were blocked by pretreatment with the MAO-B inhibitor deprenyl. Changes in the dopaminergic system parallel those observed in SOR with MPTP treatment impairing recognition memory in the absence of a deficit in odor discrimination during learning. Deprenyl pretreatment blocked the MPTP-induced impairment of SOR memory.

CONCLUSION

The use of the SOR memory model may provide a preclinical method for evaluating cognitive therapies for PD.

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Authors+Show Affiliations

Monaghan MM
Discovery Neuroscience, Pfizer Global Research and Development, CN8000, Princeton, NJ 08534, USA. monaghm@wyeth.com
Leddy L
No affiliation info available
Sung ML
No affiliation info available
Albinson K
No affiliation info available
Kubek K
No affiliation info available
Pangalos MN
No affiliation info available
Reinhart PH
No affiliation info available
Zaleska MM
No affiliation info available
Comery TA
No affiliation info available

MeSH

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAnalysis of VarianceAnimalsDisease Models, AnimalDopamineDopamine Plasma Membrane Transport ProteinsExploratory BehaviorMPTP PoisoningMaleMemory DisordersMiceMice, Inbred C57BLRecognition, PsychologySocial DominanceSubstantia NigraTyrosine 3-Monooxygenase

Pub Type(s)

Journal Article

Language

eng

PubMed ID

20197696

Citation

Monaghan, Michael M., et al. "Social Odor Recognition: a Novel Behavioral Model for Cognitive Dysfunction in Parkinson's Disease." Neuro-degenerative Diseases, vol. 7, no. 1-3, 2010, pp. 153-9.
Monaghan MM, Leddy L, Sung ML, et al. Social odor recognition: a novel behavioral model for cognitive dysfunction in Parkinson's disease. Neurodegener Dis. 2010;7(1-3):153-9.
Monaghan, M. M., Leddy, L., Sung, M. L., Albinson, K., Kubek, K., Pangalos, M. N., Reinhart, P. H., Zaleska, M. M., & Comery, T. A. (2010). Social odor recognition: a novel behavioral model for cognitive dysfunction in Parkinson's disease. Neuro-degenerative Diseases, 7(1-3), 153-9. https://doi.org/10.1159/000289227
Monaghan MM, et al. Social Odor Recognition: a Novel Behavioral Model for Cognitive Dysfunction in Parkinson's Disease. Neurodegener Dis. 2010;7(1-3):153-9. PubMed PMID: 20197696.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Social odor recognition: a novel behavioral model for cognitive dysfunction in Parkinson's disease. AU - Monaghan,Michael M, AU - Leddy,Lauren, AU - Sung,Mei-Li Amy, AU - Albinson,Kristin, AU - Kubek,Katie, AU - Pangalos,Menelas N, AU - Reinhart,Peter H, AU - Zaleska,Margaret M, AU - Comery,Thomas A, Y1 - 2010/03/03/ PY - 2010/3/4/entrez PY - 2010/3/4/pubmed PY - 2010/7/22/medline SP - 153 EP - 9 JF - Neuro-degenerative diseases JO - Neurodegener Dis VL - 7 IS - 1-3 N2 - BACKGROUND: Parkinson's disease (PD) is a progressive neurodegenerative condition characterized by an increasing loss of dopaminergic neurons resulting in motor dysfunction. However, cognitive impairments in PD patients are a common clinical feature that has gained increased attention. OBJECTIVE: The purpose of the current study was to evaluate the effects of an MPTP-induced dopaminergic lesion in mice on social odor recognition (SOR) memory. METHODS: Mice were acutely treated with MPTP and evaluated for memory impairments in the SOR assay and characterized using biochemical and immunohistochemical methods approximately 2 weeks later. RESULTS: Here we demonstrate that SOR memory is sensitive to MPTP treatment and that it correlates with multiple measures of nigrostriatal integrity. MPTP treatment of C57BL/6N mice produced a profound decrease in dopamine levels, dopamine transporter binding and tyrosine hydroxylase immunoreactivity in the striatum. These impairments in stratial dopaminergic function were blocked by pretreatment with the MAO-B inhibitor deprenyl. Changes in the dopaminergic system parallel those observed in SOR with MPTP treatment impairing recognition memory in the absence of a deficit in odor discrimination during learning. Deprenyl pretreatment blocked the MPTP-induced impairment of SOR memory. CONCLUSION: The use of the SOR memory model may provide a preclinical method for evaluating cognitive therapies for PD. SN - 1660-2862 UR - https://www.unboundmedicine.com/medline/citation/20197696/Social_odor_recognition:_a_novel_behavioral_model_for_cognitive_dysfunction_in_Parkinson's_disease_ L2 - https://www.karger.com?DOI=10.1159/000289227 DB - PRIME DP - Unbound Medicine ER -