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  1. Article: Motivational disturbances in rodent models of neuropsychiatric disorders.

    Canonica, Tara / Zalachoras, Ioannis

    Frontiers in behavioral neuroscience

    2022  Volume 16, Page(s) 940672

    Abstract: Motivated behavior is integral to the survival of individuals, continuously directing actions toward rewards or away from punishments. The orchestration of motivated behavior depends on interactions among different brain circuits, primarily within the ... ...

    Abstract Motivated behavior is integral to the survival of individuals, continuously directing actions toward rewards or away from punishments. The orchestration of motivated behavior depends on interactions among different brain circuits, primarily within the dopaminergic system, that subserve the analysis of factors such as the effort necessary for obtaining the reward and the desirability of the reward. Impairments in motivated behavior accompany a wide range of neuropsychiatric disorders, decreasing the patients' quality of life. Despite its importance, motivation is often overlooked as a parameter in neuropsychiatric disorders. Here, we review motivational impairments in rodent models of schizophrenia, depression, and Parkinson's disease, focusing on studies investigating effort-related behavior in operant conditioning tasks and on pharmacological interventions targeting the dopaminergic system. Similar motivational disturbances accompany these conditions, suggesting that treatments aimed at ameliorating motivation levels may be beneficial for various neuropsychiatric disorders.
    Language English
    Publishing date 2022-08-16
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2452960-6
    ISSN 1662-5153
    ISSN 1662-5153
    DOI 10.3389/fnbeh.2022.940672
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Motor skill learning and reward consumption differentially affect VTA activation.

    Leemburg, Susan / Canonica, Tara / Luft, Andreas

    Scientific reports

    2018  Volume 8, Issue 1, Page(s) 687

    Abstract: Dopamine release from the ventral tegmental area (VTA) terminals in the primary motor cortex (M1) enables motor skill acquisition. Here, we test the hypothesis that dopaminergic VTA neurons projecting to M1 are activated when rewards are obtained during ... ...

    Abstract Dopamine release from the ventral tegmental area (VTA) terminals in the primary motor cortex (M1) enables motor skill acquisition. Here, we test the hypothesis that dopaminergic VTA neurons projecting to M1 are activated when rewards are obtained during motor skill acquisition, but not during task execution at plateau performance, or by rewards obtained without performing skilled movements. Rats were trained to perform a skilled reaching task for 3 days (acquisition) or 7 days (plateau). In combination with retrograde labelling of VTA-to-M1 projection neurons, double immunofluorescence for c-fos and tyrosine hydroxylase (TH) was used to assess activation of dopaminergic and non-dopaminergic VTA neurons. Dopaminergic VTA-to-M1 projection neurons were indeed activated during successful motor skill acquisition, but not when rats failed to learn or had reached plateau performance, nor by food rewards alone. By contrast, dopaminergic VTA neurons that did not project to M1 were activated by both skilled reaching and food rewards. Non-dopaminergic neurons were found to be activated by motor task performance at plateau, but not during skill acquisition. These results indicate that distinct populations of VTA neurons are activated by motor skill acquisition and task performance. Moreover, this activation is not merely related to consumption of food rewards.
    MeSH term(s) Animals ; Behavior, Animal ; Dopaminergic Neurons/metabolism ; Dopaminergic Neurons/pathology ; Male ; Microscopy, Fluorescence ; Motor Skills ; Proto-Oncogene Proteins c-fos/metabolism ; Rats ; Rats, Long-Evans ; Ventral Tegmental Area/metabolism ; Ventral Tegmental Area/pathology
    Chemical Substances Proto-Oncogene Proteins c-fos
    Language English
    Publishing date 2018-01-12
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-017-18716-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Book ; Online: Motor skill learning and reward consumption differentially affect VTA activation

    Leemburg, Susan / Canonica, Tara / Luft, Andreas

    2018  

    Abstract: Dopamine release from the ventral tegmental area (VTA) terminals in the primary motor cortex (M1) enables motor skill acquisition. Here, we test the hypothesis that dopaminergic VTA neurons projecting to M1 are activated when rewards are obtained during ... ...

    Abstract Dopamine release from the ventral tegmental area (VTA) terminals in the primary motor cortex (M1) enables motor skill acquisition. Here, we test the hypothesis that dopaminergic VTA neurons projecting to M1 are activated when rewards are obtained during motor skill acquisition, but not during task execution at plateau performance, or by rewards obtained without performing skilled movements. Rats were trained to perform a skilled reaching task for 3 days (acquisition) or 7 days (plateau). In combination with retrograde labelling of VTA-to-M1 projection neurons, double immunofluorescence for c-fos and tyrosine hydroxylase (TH) was used to assess activation of dopaminergic and non-dopaminergic VTA neurons. Dopaminergic VTA-to-M1 projection neurons were indeed activated during successful motor skill acquisition, but not when rats failed to learn or had reached plateau performance, nor by food rewards alone. By contrast, dopaminergic VTA neurons that did not project to M1 were activated by both skilled reaching and food rewards. Non-dopaminergic neurons were found to be activated by motor task performance at plateau, but not during skill acquisition. These results indicate that distinct populations of VTA neurons are activated by motor skill acquisition and task performance. Moreover, this activation is not merely related to consumption of food rewards.
    Keywords Article
    Subject code 796 ; 590
    Language English
    Publishing date 2018-01-12
    Publisher Nature Publishing Group UK
    Publishing country us
    Document type Book ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Specialized astrocytes mediate glutamatergic gliotransmission in the CNS.

    de Ceglia, Roberta / Ledonne, Ada / Litvin, David Gregory / Lind, Barbara Lykke / Carriero, Giovanni / Latagliata, Emanuele Claudio / Bindocci, Erika / Di Castro, Maria Amalia / Savtchouk, Iaroslav / Vitali, Ilaria / Ranjak, Anurag / Congiu, Mauro / Canonica, Tara / Wisden, William / Harris, Kenneth / Mameli, Manuel / Mercuri, Nicola / Telley, Ludovic / Volterra, Andrea

    Nature

    2023  Volume 622, Issue 7981, Page(s) 120–129

    Abstract: Multimodal astrocyte-neuron communications govern brain circuitry assembly and ... ...

    Abstract Multimodal astrocyte-neuron communications govern brain circuitry assembly and function
    MeSH term(s) Adult ; Humans ; Astrocytes/classification ; Astrocytes/cytology ; Astrocytes/metabolism ; Central Nervous System/cytology ; Central Nervous System/metabolism ; Glutamic Acid/metabolism ; Hippocampus/cytology ; Hippocampus/metabolism ; Neurons/metabolism ; Signal Transduction ; Synaptic Transmission ; Calcium/metabolism ; Exocytosis ; Single-Cell Gene Expression Analysis ; Vesicular Glutamate Transport Protein 1/deficiency ; Vesicular Glutamate Transport Protein 1/genetics ; Gene Deletion ; Cerebral Cortex/cytology ; Cerebral Cortex/metabolism
    Chemical Substances Glutamic Acid (3KX376GY7L) ; SLC17A7 protein, human ; Calcium (SY7Q814VUP) ; Vesicular Glutamate Transport Protein 1
    Language English
    Publishing date 2023-09-06
    Publishing country England
    Document type Journal Article
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-023-06502-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 26: Show issues Location:
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  5. Article ; Online: Altered Hippocampal-Prefrontal Neural Dynamics in Mouse Models of Down Syndrome.

    Chang, Pishan / Bush, Daniel / Schorge, Stephanie / Good, Mark / Canonica, Tara / Shing, Nathanael / Noy, Suzanna / Wiseman, Frances K / Burgess, Neil / Tybulewicz, Victor L J / Walker, Matthew C / Fisher, Elizabeth M C

    Cell reports

    2020  Volume 30, Issue 4, Page(s) 1152–1163.e4

    Abstract: Altered neural dynamics in the medial prefrontal cortex (mPFC) and hippocampus may contribute to cognitive impairments in the complex chromosomal disorder Down syndrome (DS). Here, we demonstrate non-overlapping behavioral differences associated with ... ...

    Abstract Altered neural dynamics in the medial prefrontal cortex (mPFC) and hippocampus may contribute to cognitive impairments in the complex chromosomal disorder Down syndrome (DS). Here, we demonstrate non-overlapping behavioral differences associated with distinct abnormalities in hippocampal and mPFC electrophysiology during a canonical spatial working memory task in three partially trisomic mouse models of DS (Dp1Tyb, Dp10Yey, and Dp17Yey) that together cover all regions of homology with human chromosome 21 (Hsa21). Dp1Tyb mice show slower decision-making (unrelated to the gene dose of DYRK1A, which has been implicated in DS cognitive dysfunction) and altered theta dynamics (reduced frequency, increased hippocampal-mPFC coherence, and increased modulation of hippocampal high gamma); Dp10Yey mice show impaired alternation performance and reduced theta modulation of hippocampal low gamma; and Dp17Yey mice are not significantly different from the wild type. These results link specific hippocampal and mPFC circuit dysfunctions to cognitive deficits in DS models and, importantly, map them to discrete regions of Hsa21.
    MeSH term(s) Animals ; Chromosomes, Human, Pair 21/genetics ; Cognitive Dysfunction/genetics ; Cognitive Dysfunction/physiopathology ; Disease Models, Animal ; Down Syndrome/genetics ; Electroencephalography ; Hippocampus/metabolism ; Hippocampus/physiopathology ; Humans ; Male ; Memory, Short-Term/physiology ; Mice ; Mice, Inbred C57BL ; Prefrontal Cortex/metabolism ; Prefrontal Cortex/physiology ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/genetics ; Protein-Tyrosine Kinases/metabolism ; Spatial Memory/physiology ; Theta Rhythm/genetics ; Trisomy/genetics ; Trisomy/physiopathology ; Dyrk Kinases
    Chemical Substances Protein-Tyrosine Kinases (EC 2.7.10.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2020-01-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2019.12.065
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  6. Article ; Online: Comprehensive phenotypic analysis of the Dp1Tyb mouse strain reveals a broad range of Down syndrome-related phenotypes.

    Lana-Elola, Eva / Cater, Heather / Watson-Scales, Sheona / Greenaway, Simon / Müller-Winkler, Jennifer / Gibbins, Dorota / Nemes, Mihaela / Slender, Amy / Hough, Tertius / Keskivali-Bond, Piia / Scudamore, Cheryl L / Herbert, Eleanor / Banks, Gareth T / Mobbs, Helene / Canonica, Tara / Tosh, Justin / Noy, Suzanna / Llorian, Miriam / Nolan, Patrick M /
    Griffin, Julian L / Good, Mark / Simon, Michelle / Mallon, Ann-Marie / Wells, Sara / Fisher, Elizabeth M C / Tybulewicz, Victor L J

    Disease models & mechanisms

    2021  Volume 14, Issue 10

    Abstract: Down syndrome (DS), trisomy 21, results in many complex phenotypes including cognitive deficits, heart defects and craniofacial alterations. Phenotypes arise from an extra copy of human chromosome 21 (Hsa21) genes. However, these dosage-sensitive ... ...

    Abstract Down syndrome (DS), trisomy 21, results in many complex phenotypes including cognitive deficits, heart defects and craniofacial alterations. Phenotypes arise from an extra copy of human chromosome 21 (Hsa21) genes. However, these dosage-sensitive causative genes remain unknown. Animal models enable identification of genes and pathological mechanisms. The Dp1Tyb mouse model of DS has an extra copy of 63% of Hsa21-orthologous mouse genes. In order to establish whether this model recapitulates DS phenotypes, we comprehensively phenotyped Dp1Tyb mice using 28 tests of different physiological systems and found that 468 out of 1800 parameters were significantly altered. We show that Dp1Tyb mice have wide-ranging DS-like phenotypes, including aberrant erythropoiesis and megakaryopoiesis, reduced bone density, craniofacial changes, altered cardiac function, a pre-diabetic state, and deficits in memory, locomotion, hearing and sleep. Thus, Dp1Tyb mice are an excellent model for investigating complex DS phenotype-genotype relationships for this common disorder.
    MeSH term(s) Amyloid beta-Peptides/metabolism ; Anemia/complications ; Animals ; Bone Development ; Disease Models, Animal ; Down Syndrome/genetics ; Down Syndrome/pathology ; Down Syndrome/physiopathology ; Erythropoiesis ; Evoked Potentials, Auditory, Brain Stem ; Gene Expression Regulation ; Genes, Duplicate ; Hearing ; Heart Function Tests ; Hippocampus/pathology ; Locomotion ; Memory/physiology ; Mice, Inbred C57BL ; Otitis Media/complications ; Otitis Media/pathology ; Otitis Media/physiopathology ; Phenotype ; Prediabetic State/complications ; Prediabetic State/pathology ; Prediabetic State/physiopathology ; Respiration ; Sleep/physiology ; Spleen/pathology ; Splenomegaly/complications ; Mice
    Chemical Substances Amyloid beta-Peptides
    Language English
    Publishing date 2021-10-15
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.049157
    Database MEDical Literature Analysis and Retrieval System OnLINE

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