Eliminating the VGlut2-Dependent Glutamatergic Transmission of Parvalbumin-Expressing Neurons Leads to Deficits in Locomotion and Vocalization, Decreased Pain Sensitivity, and Increased Dominance
The calcium-binding protein parvalbumin (PV) is a recognized marker of short-axon GABA-ergic neurons in the cortex and the hippocampus. However in addition, PV is expressed by excitatory, glutamatergic neurons in various areas of the brain and spinal cord. Depending on the location of these neurons,...
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Frontiers Media S.A.
2018-07-01
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| Series: | Frontiers in Behavioral Neuroscience |
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| Online Access: | https://www.frontiersin.org/article/10.3389/fnbeh.2018.00146/full |
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| author | Diana M. Roccaro-Waldmeyer Franck Girard Daniele Milani Elisabetta Vannoni Laurent Prétôt David P. Wolfer David P. Wolfer David P. Wolfer Marco R. Celio |
| author_facet | Diana M. Roccaro-Waldmeyer Franck Girard Daniele Milani Elisabetta Vannoni Laurent Prétôt David P. Wolfer David P. Wolfer David P. Wolfer Marco R. Celio |
| author_sort | Diana M. Roccaro-Waldmeyer |
| collection | DOAJ |
| description | The calcium-binding protein parvalbumin (PV) is a recognized marker of short-axon GABA-ergic neurons in the cortex and the hippocampus. However in addition, PV is expressed by excitatory, glutamatergic neurons in various areas of the brain and spinal cord. Depending on the location of these neurons, loading of their synaptic vesicles with glutamate is mediated by either of three vesicular glutamate transporters (VGlut): VGlut1, VGlut2, or VGlut3. Driven by our interest in one of these glutamatergic/PV-expressing cell clusters—the lateral hypothalamic parvafox nucleus—we investigated the functions of this population of neurons by the selective deletion of VGlut2 expression in PV-expressing cells according to the Cre/Lox-approach. PV-Cre;VGlut2-Lox mutant mice are phenotypically characterized by deficits in locomotion and vocalization, by a decreased thermal nociception, and by an increased social dominance. We conducted a search of the Allen Brain Atlas for regions that might co-express the genes encoding PV and VGlut2, and that might thus contribute to the manifestation of the observed phenotypes. Our survey revealed several structures that could contribute to the deficits in locomotion and vocalization, such as the red, the subthalamic and the deep cerebellar nuclei. It also disclosed that a shift in the balance of afferental glutamatergic neurotransmission to the periaqueductal gray matter might be accountable for the decrease in sensitivity to pain and for the increase in social dominance. As a whole, this study broadens the state of knowledge about PV-expressing excitatory neurons. |
| first_indexed | 2024-12-12T09:54:53Z |
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| institution | Directory Open Access Journal |
| issn | 1662-5153 |
| language | English |
| last_indexed | 2024-12-12T09:54:53Z |
| publishDate | 2018-07-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Behavioral Neuroscience |
| spelling | doaj.art-7bd515276f9a413f85938d467d3112d62022-12-22T00:28:10ZengFrontiers Media S.A.Frontiers in Behavioral Neuroscience1662-51532018-07-011210.3389/fnbeh.2018.00146376110Eliminating the VGlut2-Dependent Glutamatergic Transmission of Parvalbumin-Expressing Neurons Leads to Deficits in Locomotion and Vocalization, Decreased Pain Sensitivity, and Increased DominanceDiana M. Roccaro-Waldmeyer0Franck Girard1Daniele Milani2Elisabetta Vannoni3Laurent Prétôt4David P. Wolfer5David P. Wolfer6David P. Wolfer7Marco R. Celio8Anatomy and Programme in Neuroscience, Department of Medicine, University of Fribourg, Fribourg, SwitzerlandAnatomy and Programme in Neuroscience, Department of Medicine, University of Fribourg, Fribourg, SwitzerlandAnatomy and Programme in Neuroscience, Department of Medicine, University of Fribourg, Fribourg, SwitzerlandDivision of Functional Neuroanatomy, Institute of Anatomy, Department of Medicine, University of Zurich, Zurich, SwitzerlandAnatomy and Programme in Neuroscience, Department of Medicine, University of Fribourg, Fribourg, SwitzerlandDivision of Functional Neuroanatomy, Institute of Anatomy, Department of Medicine, University of Zurich, Zurich, SwitzerlandInstitute of Human Movement Sciences and Sport, Department of Health Sciences and Technology, ETH Zurich, Zurich, SwitzerlandNeuroscience Center Zurich, University of Zurich and ETH Zurich, Zurich, SwitzerlandAnatomy and Programme in Neuroscience, Department of Medicine, University of Fribourg, Fribourg, SwitzerlandThe calcium-binding protein parvalbumin (PV) is a recognized marker of short-axon GABA-ergic neurons in the cortex and the hippocampus. However in addition, PV is expressed by excitatory, glutamatergic neurons in various areas of the brain and spinal cord. Depending on the location of these neurons, loading of their synaptic vesicles with glutamate is mediated by either of three vesicular glutamate transporters (VGlut): VGlut1, VGlut2, or VGlut3. Driven by our interest in one of these glutamatergic/PV-expressing cell clusters—the lateral hypothalamic parvafox nucleus—we investigated the functions of this population of neurons by the selective deletion of VGlut2 expression in PV-expressing cells according to the Cre/Lox-approach. PV-Cre;VGlut2-Lox mutant mice are phenotypically characterized by deficits in locomotion and vocalization, by a decreased thermal nociception, and by an increased social dominance. We conducted a search of the Allen Brain Atlas for regions that might co-express the genes encoding PV and VGlut2, and that might thus contribute to the manifestation of the observed phenotypes. Our survey revealed several structures that could contribute to the deficits in locomotion and vocalization, such as the red, the subthalamic and the deep cerebellar nuclei. It also disclosed that a shift in the balance of afferental glutamatergic neurotransmission to the periaqueductal gray matter might be accountable for the decrease in sensitivity to pain and for the increase in social dominance. As a whole, this study broadens the state of knowledge about PV-expressing excitatory neurons.https://www.frontiersin.org/article/10.3389/fnbeh.2018.00146/fullparvalbuminVGlut2Cre/Lox-systempainultrasonic vocalizationdominance |
| spellingShingle | Diana M. Roccaro-Waldmeyer Franck Girard Daniele Milani Elisabetta Vannoni Laurent Prétôt David P. Wolfer David P. Wolfer David P. Wolfer Marco R. Celio Eliminating the VGlut2-Dependent Glutamatergic Transmission of Parvalbumin-Expressing Neurons Leads to Deficits in Locomotion and Vocalization, Decreased Pain Sensitivity, and Increased Dominance Frontiers in Behavioral Neuroscience parvalbumin VGlut2 Cre/Lox-system pain ultrasonic vocalization dominance |
| title | Eliminating the VGlut2-Dependent Glutamatergic Transmission of Parvalbumin-Expressing Neurons Leads to Deficits in Locomotion and Vocalization, Decreased Pain Sensitivity, and Increased Dominance |
| title_full | Eliminating the VGlut2-Dependent Glutamatergic Transmission of Parvalbumin-Expressing Neurons Leads to Deficits in Locomotion and Vocalization, Decreased Pain Sensitivity, and Increased Dominance |
| title_fullStr | Eliminating the VGlut2-Dependent Glutamatergic Transmission of Parvalbumin-Expressing Neurons Leads to Deficits in Locomotion and Vocalization, Decreased Pain Sensitivity, and Increased Dominance |
| title_full_unstemmed | Eliminating the VGlut2-Dependent Glutamatergic Transmission of Parvalbumin-Expressing Neurons Leads to Deficits in Locomotion and Vocalization, Decreased Pain Sensitivity, and Increased Dominance |
| title_short | Eliminating the VGlut2-Dependent Glutamatergic Transmission of Parvalbumin-Expressing Neurons Leads to Deficits in Locomotion and Vocalization, Decreased Pain Sensitivity, and Increased Dominance |
| title_sort | eliminating the vglut2 dependent glutamatergic transmission of parvalbumin expressing neurons leads to deficits in locomotion and vocalization decreased pain sensitivity and increased dominance |
| topic | parvalbumin VGlut2 Cre/Lox-system pain ultrasonic vocalization dominance |
| url | https://www.frontiersin.org/article/10.3389/fnbeh.2018.00146/full |
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