Olfactory discrimination deficits in mice lacking the dopamine transporter or the D2 dopamine receptor
Previous pharmacological studies have implicated dopamine as a modulator of olfactory bulb processing. Several disorders characterized by altered dopamine homeostasis in olfaction-related brain regions display olfactory deficits. To further characterize the role of dopamine in olfactory processing,...
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| Veröffentlicht in: | Behavioural brain research 2006-09, Vol.172 (1), p.97-105 |
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| creator | Tillerson, Jennifer L. Caudle, W. Michael Parent, Jack M. Gong, C. Schallert, Timothy Miller, Gary W. |
| description | Previous pharmacological studies have implicated dopamine as a modulator of olfactory bulb processing. Several disorders characterized by altered dopamine homeostasis in olfaction-related brain regions display olfactory deficits. To further characterize the role of dopamine in olfactory processing, we subjected dopamine transporter knockout mice (DAT −/−) and dopamine receptor 2 knockout mice (D2 −/−) to a battery of olfactory tests. In addition to behavioral characterization, several neurochemical markers of olfactory bulb integrity and function were examined. DAT −/− mice displayed an olfactory discrimination deficit, but did not differ detectably from DAT wildtype (DAT +/+) mice in odor habituation, olfactory sensitivity, or odor recognition memory. Neurochemically, DAT −/− mice have decreased D2 receptor staining in the periglomerular layer of the olfactory bulb and increased tyrosine hydroxylase immunoreactivity compared to DAT +/+ controls. D2 −/− mice exhibited the same olfactory deficit as the DAT −/− mice, further supporting the role of dopamine at the D2 synapse in olfactory discrimination processing. The findings presented in this paper reinforce the functional significance of dopamine and more specifically the D2 receptor in olfactory discrimination and may help explain the behavioral phenotype in the DAT and D2 knockout mice. |
| doi_str_mv | 10.1016/j.bbr.2006.04.025 |
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Michael ; Parent, Jack M. ; Gong, C. ; Schallert, Timothy ; Miller, Gary W.</creator><creatorcontrib>Tillerson, Jennifer L. ; Caudle, W. Michael ; Parent, Jack M. ; Gong, C. ; Schallert, Timothy ; Miller, Gary W.</creatorcontrib><description>Previous pharmacological studies have implicated dopamine as a modulator of olfactory bulb processing. Several disorders characterized by altered dopamine homeostasis in olfaction-related brain regions display olfactory deficits. To further characterize the role of dopamine in olfactory processing, we subjected dopamine transporter knockout mice (DAT −/−) and dopamine receptor 2 knockout mice (D2 −/−) to a battery of olfactory tests. In addition to behavioral characterization, several neurochemical markers of olfactory bulb integrity and function were examined. DAT −/− mice displayed an olfactory discrimination deficit, but did not differ detectably from DAT wildtype (DAT +/+) mice in odor habituation, olfactory sensitivity, or odor recognition memory. Neurochemically, DAT −/− mice have decreased D2 receptor staining in the periglomerular layer of the olfactory bulb and increased tyrosine hydroxylase immunoreactivity compared to DAT +/+ controls. D2 −/− mice exhibited the same olfactory deficit as the DAT −/− mice, further supporting the role of dopamine at the D2 synapse in olfactory discrimination processing. The findings presented in this paper reinforce the functional significance of dopamine and more specifically the D2 receptor in olfactory discrimination and may help explain the behavioral phenotype in the DAT and D2 knockout mice.</description><identifier>ISSN: 0166-4328</identifier><identifier>EISSN: 1872-7549</identifier><identifier>DOI: 10.1016/j.bbr.2006.04.025</identifier><identifier>PMID: 16765459</identifier><identifier>CODEN: BBREDI</identifier><language>eng</language><publisher>Shannon: Elsevier B.V</publisher><subject>Animals ; Antimetabolites ; Behavioral psychophysiology ; Biological and medical sciences ; Bromodeoxyuridine ; D2 receptor ; Discrimination (Psychology) - physiology ; Discrimination Learning ; Dopamine ; Dopamine Plasma Membrane Transport Proteins - genetics ; Dopamine Plasma Membrane Transport Proteins - physiology ; Dopamine transporter ; Fundamental and applied biological sciences. Psychology ; Habituation, Psychophysiologic - physiology ; Immunohistochemistry ; Knockout mice ; Memory - physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurotransmission and behavior ; Olfaction ; Olfactory Bulb - physiology ; Olfactory discrimination ; Olfactory system and olfaction. Gustatory system and gustation ; Psychology. Psychoanalysis. Psychiatry ; Psychology. 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Michael</creatorcontrib><creatorcontrib>Parent, Jack M.</creatorcontrib><creatorcontrib>Gong, C.</creatorcontrib><creatorcontrib>Schallert, Timothy</creatorcontrib><creatorcontrib>Miller, Gary W.</creatorcontrib><title>Olfactory discrimination deficits in mice lacking the dopamine transporter or the D2 dopamine receptor</title><title>Behavioural brain research</title><addtitle>Behav Brain Res</addtitle><description>Previous pharmacological studies have implicated dopamine as a modulator of olfactory bulb processing. Several disorders characterized by altered dopamine homeostasis in olfaction-related brain regions display olfactory deficits. To further characterize the role of dopamine in olfactory processing, we subjected dopamine transporter knockout mice (DAT −/−) and dopamine receptor 2 knockout mice (D2 −/−) to a battery of olfactory tests. In addition to behavioral characterization, several neurochemical markers of olfactory bulb integrity and function were examined. DAT −/− mice displayed an olfactory discrimination deficit, but did not differ detectably from DAT wildtype (DAT +/+) mice in odor habituation, olfactory sensitivity, or odor recognition memory. Neurochemically, DAT −/− mice have decreased D2 receptor staining in the periglomerular layer of the olfactory bulb and increased tyrosine hydroxylase immunoreactivity compared to DAT +/+ controls. D2 −/− mice exhibited the same olfactory deficit as the DAT −/− mice, further supporting the role of dopamine at the D2 synapse in olfactory discrimination processing. The findings presented in this paper reinforce the functional significance of dopamine and more specifically the D2 receptor in olfactory discrimination and may help explain the behavioral phenotype in the DAT and D2 knockout mice.</description><subject>Animals</subject><subject>Antimetabolites</subject><subject>Behavioral psychophysiology</subject><subject>Biological and medical sciences</subject><subject>Bromodeoxyuridine</subject><subject>D2 receptor</subject><subject>Discrimination (Psychology) - physiology</subject><subject>Discrimination Learning</subject><subject>Dopamine</subject><subject>Dopamine Plasma Membrane Transport Proteins - genetics</subject><subject>Dopamine Plasma Membrane Transport Proteins - physiology</subject><subject>Dopamine transporter</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Habituation, Psychophysiologic - physiology</subject><subject>Immunohistochemistry</subject><subject>Knockout mice</subject><subject>Memory - physiology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Neurotransmission and behavior</subject><subject>Olfaction</subject><subject>Olfactory Bulb - physiology</subject><subject>Olfactory discrimination</subject><subject>Olfactory system and olfaction. Gustatory system and gustation</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychology. Psychophysiology</subject><subject>Receptors, Dopamine D2 - genetics</subject><subject>Receptors, Dopamine D2 - physiology</subject><subject>Recognition memory</subject><subject>Smell - physiology</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0166-4328</issn><issn>1872-7549</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1v3CAQhlHVqtmk_QG5VFyam10wX0Y5RWk-KkXKpTkjDOOWjde4wFbKvw-bXWlvOQ3SPPMO8yB0TklLCZU_1u0wpLYjRLaEt6QTH9CK9qprlOD6I1pVRjacdf0JOs15TQjhRNDP6IRKJQUXeoXGx2m0rsT0gn3ILoVNmG0JccYexuBCyTjMeBMc4Mm65zD_weUvYB8XW0nAJdk5LzEVSDimt97P7thO4GCp6V_Qp9FOGb4e6hl6ur35fX3fPDze_bq-emgcV31p1NhJyb3QTDDmBCXaawuKjlIy6Rmrz0E5Tgdne604B8JAW6cpd13fKWBn6GKfu6T4bwu5mE29CqbJzhC32VDNCBWEVZDuQZdizglGs9TbbXoxlJidXLM2Va7ZyTWEmyq3znw7hG-HDfjjxMFmBb4fAJudncbqxoV85JRWmojd8ss9B1XF_wDJZBdgduBDFVaMj-Gdb7wC2OSXgw</recordid><startdate>20060915</startdate><enddate>20060915</enddate><creator>Tillerson, Jennifer L.</creator><creator>Caudle, W. 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Michael ; Parent, Jack M. ; Gong, C. ; Schallert, Timothy ; Miller, Gary W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c478t-7f2664d593533c5109d9ae71f6636d33e71b7c41bca89744e03e9ac914c2827e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Antimetabolites</topic><topic>Behavioral psychophysiology</topic><topic>Biological and medical sciences</topic><topic>Bromodeoxyuridine</topic><topic>D2 receptor</topic><topic>Discrimination (Psychology) - physiology</topic><topic>Discrimination Learning</topic><topic>Dopamine</topic><topic>Dopamine Plasma Membrane Transport Proteins - genetics</topic><topic>Dopamine Plasma Membrane Transport Proteins - physiology</topic><topic>Dopamine transporter</topic><topic>Fundamental and applied biological sciences. 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Michael</creatorcontrib><creatorcontrib>Parent, Jack M.</creatorcontrib><creatorcontrib>Gong, C.</creatorcontrib><creatorcontrib>Schallert, Timothy</creatorcontrib><creatorcontrib>Miller, Gary W.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Neurosciences Abstracts</collection><jtitle>Behavioural brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tillerson, Jennifer L.</au><au>Caudle, W. Michael</au><au>Parent, Jack M.</au><au>Gong, C.</au><au>Schallert, Timothy</au><au>Miller, Gary W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Olfactory discrimination deficits in mice lacking the dopamine transporter or the D2 dopamine receptor</atitle><jtitle>Behavioural brain research</jtitle><addtitle>Behav Brain Res</addtitle><date>2006-09-15</date><risdate>2006</risdate><volume>172</volume><issue>1</issue><spage>97</spage><epage>105</epage><pages>97-105</pages><issn>0166-4328</issn><eissn>1872-7549</eissn><coden>BBREDI</coden><abstract>Previous pharmacological studies have implicated dopamine as a modulator of olfactory bulb processing. Several disorders characterized by altered dopamine homeostasis in olfaction-related brain regions display olfactory deficits. To further characterize the role of dopamine in olfactory processing, we subjected dopamine transporter knockout mice (DAT −/−) and dopamine receptor 2 knockout mice (D2 −/−) to a battery of olfactory tests. In addition to behavioral characterization, several neurochemical markers of olfactory bulb integrity and function were examined. DAT −/− mice displayed an olfactory discrimination deficit, but did not differ detectably from DAT wildtype (DAT +/+) mice in odor habituation, olfactory sensitivity, or odor recognition memory. Neurochemically, DAT −/− mice have decreased D2 receptor staining in the periglomerular layer of the olfactory bulb and increased tyrosine hydroxylase immunoreactivity compared to DAT +/+ controls. D2 −/− mice exhibited the same olfactory deficit as the DAT −/− mice, further supporting the role of dopamine at the D2 synapse in olfactory discrimination processing. The findings presented in this paper reinforce the functional significance of dopamine and more specifically the D2 receptor in olfactory discrimination and may help explain the behavioral phenotype in the DAT and D2 knockout mice.</abstract><cop>Shannon</cop><pub>Elsevier B.V</pub><pmid>16765459</pmid><doi>10.1016/j.bbr.2006.04.025</doi><tpages>9</tpages></addata></record> |
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| subjects | Animals Antimetabolites Behavioral psychophysiology Biological and medical sciences Bromodeoxyuridine D2 receptor Discrimination (Psychology) - physiology Discrimination Learning Dopamine Dopamine Plasma Membrane Transport Proteins - genetics Dopamine Plasma Membrane Transport Proteins - physiology Dopamine transporter Fundamental and applied biological sciences. Psychology Habituation, Psychophysiologic - physiology Immunohistochemistry Knockout mice Memory - physiology Mice Mice, Inbred C57BL Mice, Knockout Neurotransmission and behavior Olfaction Olfactory Bulb - physiology Olfactory discrimination Olfactory system and olfaction. Gustatory system and gustation Psychology. Psychoanalysis. Psychiatry Psychology. Psychophysiology Receptors, Dopamine D2 - genetics Receptors, Dopamine D2 - physiology Recognition memory Smell - physiology Vertebrates: nervous system and sense organs |
| title | Olfactory discrimination deficits in mice lacking the dopamine transporter or the D2 dopamine receptor |
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