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  1. Article ; Online: Reliable, Fast and Stable Contrast Response Function Estimation.

    Cortes, Nelson / Demers, Marc / Ady, Visou / Ikan, Lamyae / Casanova, Christian

    Vision (Basel, Switzerland)

    2022  Volume 6, Issue 4

    Abstract: A study was conducted to determine stable cortical contrast response functions (CRFs) accurately and repeatedly in the shortest possible experimentation time. The method consisted of searching for experimental temporal aspects (number and duration of ... ...

    Abstract A study was conducted to determine stable cortical contrast response functions (CRFs) accurately and repeatedly in the shortest possible experimentation time. The method consisted of searching for experimental temporal aspects (number and duration of trials and number and distribution of contrasts used) with a model based on inhomogeneous Poisson spike trains to varying contrast levels. The set of values providing both short experimental duration and maximizing fit of the CRFs were saved, and then tested on cats' visual cortical neurons. Our analysis revealed that 4 sets of parameters with less or equal to 6 experimental visual contrasts satisfied our premise of obtaining good CRFs' performance in a short recording period, in which the number of trials seems to be the experimental condition that stabilizes the fit.
    Language English
    Publishing date 2022-10-17
    Publishing country Switzerland
    Document type Journal Article
    ISSN 2411-5150
    ISSN (online) 2411-5150
    DOI 10.3390/vision6040062
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: New old drug(s) for spinocerebellar ataxias.

    Ady, Visou / Watt, Alanna J

    The Journal of physiology

    2017  Volume 595, Issue 1, Page(s) 5–6

    Language English
    Publishing date 2017-01-01
    Publishing country England
    Document type Journal Article
    ZDB-ID 3115-x
    ISSN 1469-7793 ; 0022-3751
    ISSN (online) 1469-7793
    ISSN 0022-3751
    DOI 10.1113/JP273149
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uc I Zs.65: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Altered synaptic and firing properties of cerebellar Purkinje cells in a mouse model of ARSACS.

    Ady, Visou / Toscano-Márquez, Brenda / Nath, Moushumi / Chang, Philip K / Hui, Jeanette / Cook, Anna / Charron, François / Larivière, Roxanne / Brais, Bernard / McKinney, R Anne / Watt, Alanna J

    The Journal of physiology

    2018  Volume 596, Issue 17, Page(s) 4253–4267

    Abstract: Key points: Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is an early-onset neurodegenerative human disease characterized in part by ataxia and Purkinje cell loss in anterior cerebellar lobules. A knock-out mouse model has been ... ...

    Abstract Key points: Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is an early-onset neurodegenerative human disease characterized in part by ataxia and Purkinje cell loss in anterior cerebellar lobules. A knock-out mouse model has been developed that recapitulates several features of ARSACS. Using this ARSACS mouse model, we report changes in synaptic input and intrinsic firing in cerebellar Purkinje cells, as well as in their synaptic output in the deep cerebellar nuclei. Changes in firing are observed in anterior lobules that later exhibit Purkinje cell death, but not in posterior lobules that do not. Our results show that both synaptic and intrinsic alterations in Purkinje cell properties likely contribute to disease manifestation in ARSACS; these findings resemble pathophysiological changes reported in several other ataxias.
    Abstract: Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is an early-onset neurodegenerative disease that includes a pronounced and progressive cerebellar dysfunction. ARSACS is caused by an autosomal recessive loss-of-function mutation in the Sacs gene that encodes the protein sacsin. To better understand the cerebellar pathophysiology in ARSACS, we studied synaptic and firing properties of Purkinje cells from a mouse model of ARSACS, Sacs
    MeSH term(s) Animals ; Behavior, Animal ; Cerebellar Ataxia/physiopathology ; Disease Models, Animal ; Heat-Shock Proteins/physiology ; Humans ; Mice ; Mice, Knockout ; Muscle Spasticity/physiopathology ; Mutation ; Purkinje Cells/cytology ; Purkinje Cells/physiology ; Spinocerebellar Ataxias/congenital ; Spinocerebellar Ataxias/physiopathology ; Synapses/physiology
    Chemical Substances Heat-Shock Proteins ; Sacs protein, mouse
    Language English
    Publishing date 2018-07-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3115-x
    ISSN 1469-7793 ; 0022-3751
    ISSN (online) 1469-7793
    ISSN 0022-3751
    DOI 10.1113/JP275902
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.65: Show issues Location:
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  4. Article ; Online: Type 1 metabotropic glutamate receptors (mGlu1) trigger the gating of GluD2 delta glutamate receptors.

    Ady, Visou / Perroy, Julie / Tricoire, Ludovic / Piochon, Claire / Dadak, Selma / Chen, Xiaoru / Dusart, Isabelle / Fagni, Laurent / Lambolez, Bertrand / Levenes, Carole

    EMBO reports

    2013  Volume 15, Issue 1, Page(s) 103–109

    Abstract: The orphan GluD2 receptor belongs to the ionotropic glutamate receptor family but does not bind glutamate. Ligand-gated GluD2 currents have never been evidenced, and whether GluD2 operates as an ion channel has been a long-standing question. Here, we ... ...

    Abstract The orphan GluD2 receptor belongs to the ionotropic glutamate receptor family but does not bind glutamate. Ligand-gated GluD2 currents have never been evidenced, and whether GluD2 operates as an ion channel has been a long-standing question. Here, we show that GluD2 gating is triggered by type 1 metabotropic glutamate receptors, both in a heterologous expression system and in Purkinje cells. Thus, GluD2 is not only an adhesion molecule at synapses but also works as a channel. This gating mechanism reveals new properties of glutamate receptors that emerge from their interaction and opens unexpected perspectives regarding synaptic transmission and plasticity.
    MeSH term(s) Animals ; Calcium Signaling ; Cerebellum/cytology ; Excitatory Amino Acid Agonists/pharmacology ; Excitatory Postsynaptic Potentials ; Glycine/analogs & derivatives ; Glycine/pharmacology ; HEK293 Cells ; Humans ; Ion Channel Gating ; Male ; Mice ; Mice, Inbred C57BL ; Purkinje Fibers/drug effects ; Purkinje Fibers/physiology ; Receptors, Glutamate/metabolism ; Receptors, Metabotropic Glutamate/metabolism ; Resorcinols/pharmacology
    Chemical Substances Excitatory Amino Acid Agonists ; Receptors, Glutamate ; Receptors, Metabotropic Glutamate ; Resorcinols ; glutamate receptor delta 2 ; 3,5-dihydroxyphenylglycine (5YR2N37E6D) ; Glycine (TE7660XO1C)
    Language English
    Publishing date 2013-12-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2020896-0
    ISSN 1469-3178 ; 1469-221X
    ISSN (online) 1469-3178
    ISSN 1469-221X
    DOI 10.1002/embr.201337371
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Jg. 1995 - 2021: Lesesall (2.OG)
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