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Olfactory behavior and physiology are disrupted in prion protein knockout mice.

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Title: Olfactory behavior and physiology are disrupted in prion protein knockout mice.
Authors: Le Pichon, Claire E., Valley, Matthew T., Polymenidou, Magdalini, Chesler, Alexander T., Sagdullaev, Botir T., Aguzzi, Adriano, Firestein, Stuart
Source: Nature Neuroscience. Jan2009, Vol. 12 Issue 1, p60-69. 10p. 1 Diagram, 1 Chart, 7 Graphs.
Subjects: Prion diseases, Smell, Mice genetics, Phenotypes, Neural transmission, Genetics
Abstract: The prion protein PrPC is infamous for its role in disease, but its normal physiological function remains unknown. Here we found a previously unknown behavioral phenotype of Prnp−/− mice in an odor-guided task. This phenotype was manifest in three Prnp knockout lines on different genetic backgrounds, which provides strong evidence that the phenotype is caused by a lack of PrPC rather than by other genetic factors. Prnp−/− mice also showed altered behavior in a second olfactory task, suggesting that the phenotype is olfactory specific. Furthermore, PrPC deficiency affected oscillatory activity in the deep layers of the main olfactory bulb, as well as dendrodendritic synaptic transmission between olfactory bulb granule and mitral cells. Notably, both the behavioral and electrophysiological alterations found in Prnp−/− mice were rescued by transgenic neuronal-specific expression of PrPC. These data suggest that PrPC is important in the normal processing of sensory information by the olfactory system. [ABSTRACT FROM AUTHOR]
Copyright of Nature Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Olfactory behavior and physiology are disrupted in prion protein knockout mice.
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  Data: <searchLink fieldCode="AR" term="%22Le+Pichon%2C+Claire+E%2E%22">Le Pichon, Claire E.</searchLink><br /><searchLink fieldCode="AR" term="%22Valley%2C+Matthew+T%2E%22">Valley, Matthew T.</searchLink><br /><searchLink fieldCode="AR" term="%22Polymenidou%2C+Magdalini%22">Polymenidou, Magdalini</searchLink><br /><searchLink fieldCode="AR" term="%22Chesler%2C+Alexander+T%2E%22">Chesler, Alexander T.</searchLink><br /><searchLink fieldCode="AR" term="%22Sagdullaev%2C+Botir+T%2E%22">Sagdullaev, Botir T.</searchLink><br /><searchLink fieldCode="AR" term="%22Aguzzi%2C+Adriano%22">Aguzzi, Adriano</searchLink><br /><searchLink fieldCode="AR" term="%22Firestein%2C+Stuart%22">Firestein, Stuart</searchLink>
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  Data: <searchLink fieldCode="DE" term="%22Prion+diseases%22">Prion diseases</searchLink><br /><searchLink fieldCode="DE" term="%22Smell%22">Smell</searchLink><br /><searchLink fieldCode="DE" term="%22Mice+genetics%22">Mice genetics</searchLink><br /><searchLink fieldCode="DE" term="%22Phenotypes%22">Phenotypes</searchLink><br /><searchLink fieldCode="DE" term="%22Neural+transmission%22">Neural transmission</searchLink><br /><searchLink fieldCode="DE" term="%22Genetics%22">Genetics</searchLink>
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  Data: The prion protein PrPC is infamous for its role in disease, but its normal physiological function remains unknown. Here we found a previously unknown behavioral phenotype of Prnp−/− mice in an odor-guided task. This phenotype was manifest in three Prnp knockout lines on different genetic backgrounds, which provides strong evidence that the phenotype is caused by a lack of PrPC rather than by other genetic factors. Prnp−/− mice also showed altered behavior in a second olfactory task, suggesting that the phenotype is olfactory specific. Furthermore, PrPC deficiency affected oscillatory activity in the deep layers of the main olfactory bulb, as well as dendrodendritic synaptic transmission between olfactory bulb granule and mitral cells. Notably, both the behavioral and electrophysiological alterations found in Prnp−/− mice were rescued by transgenic neuronal-specific expression of PrPC. These data suggest that PrPC is important in the normal processing of sensory information by the olfactory system. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Nature Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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