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000151528 0247_ $$2doi$$a10.1523/JNEUROSCI.2316-19.2020
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000151528 0247_ $$2ISSN$$a1529-2401
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000151528 041__ $$aEnglish
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000151528 1001_ $$0P:(DE-2719)2811704$$aFalck, Joanne$$b0$$eFirst author
000151528 245__ $$aLoss of Piccolo Function in Rats Induces Cerebellar Network Dysfunction and Pontocerebellar Hypoplasia Type 3-like Phenotypes
000151528 260__ $$aWashington, DC$$bSoc.8825$$c2020
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000151528 520__ $$aPiccolo, a presynaptic active zone protein, is best known for its role in the regulated assembly and function of vertebrate synapses. Genetic studies suggest a further link to several psychiatric disorders as well as Pontocerebellar Hypoplasia type 3 (PCH3). We have characterized recently generated Piccolo KO (Pclogt/gt) rats. Analysis of rats of both sexes revealed a dramatic reduction in brain size compared with WT (Pclowt/wt) animals, attributed to a decrease in the size of the cerebral cortical, cerebellar, and pontine regions. Analysis of the cerebellum and brainstem revealed a reduced granule cell layer and a reduction in size of pontine nuclei. Moreover, the maturation of mossy fiber afferents from pontine neurons and the expression of the α6 GABAA receptor subunit at the mossy fiber-granule cell synapse are perturbed, as well as the innervation of Purkinje cells by cerebellar climbing fibers. Ultrastructural and functional studies revealed a reduced size of mossy fiber boutons, with fewer synaptic vesicles and altered synaptic transmission. These data imply that Piccolo is required for the normal development, maturation, and function of neuronal networks formed between the brainstem and cerebellum. Consistently, behavioral studies demonstrated that adult Pclogt/gt rats display impaired motor coordination, despite adequate performance in tasks that reflect muscle strength and locomotion. Together, these data suggest that loss of Piccolo function in patients with PCH3 could be involved in many of the observed anatomical and behavioral symptoms, and that the further analysis of these animals could provide fundamental mechanistic insights into this devastating disorder.
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000151528 542__ $$2Crossref$$i2020-10-01$$uhttps://creativecommons.org/licenses/by-nc-sa/4.0/
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000151528 650_2 $$2MeSH$$aAnimals
000151528 650_2 $$2MeSH$$aCerebellum: metabolism
000151528 650_2 $$2MeSH$$aCerebellum: pathology
000151528 650_2 $$2MeSH$$aCerebellum: physiopathology
000151528 650_2 $$2MeSH$$aCytoskeletal Proteins: metabolism
000151528 650_2 $$2MeSH$$aDisease Models, Animal
000151528 650_2 $$2MeSH$$aFemale
000151528 650_2 $$2MeSH$$aGene Knockout Techniques
000151528 650_2 $$2MeSH$$aMale
000151528 650_2 $$2MeSH$$aNeuropeptides: metabolism
000151528 650_2 $$2MeSH$$aOlivopontocerebellar Atrophies
000151528 650_2 $$2MeSH$$aPhenotype
000151528 650_2 $$2MeSH$$aRats
000151528 7001_ $$0P:(DE-2719)2811027$$aBruns, Christine$$b1
000151528 7001_ $$0P:(DE-2719)2811236$$aHoffmann, Sheila Sook-Hi$$b2
000151528 7001_ $$aStraub, Isabelle$$b3
000151528 7001_ $$aPlautz, Erik J.$$b4
000151528 7001_ $$aOrlando, Marta$$b5
000151528 7001_ $$aMunawar, Humaira$$b6
000151528 7001_ $$aRivalan, Marion$$b7
000151528 7001_ $$aWinter, York$$b8
000151528 7001_ $$aIzsvák, Zsuzsanna$$b9
000151528 7001_ $$0P:(DE-HGF)0$$aSchmitz, Dietmar$$b10
000151528 7001_ $$aHamra, F. Kent$$b11
000151528 7001_ $$aHallermann, Stefan$$b12
000151528 7001_ $$0P:(DE-2719)2810922$$aGarner, Craig Curtis$$b13$$eCorresponding author
000151528 7001_ $$0P:(DE-2719)2810967$$aAckermann, Frauke$$b14$$eLast author
000151528 77318 $$2Crossref$$3journal-article$$a10.1523/jneurosci.2316-19.2020$$bSociety for Neuroscience$$d2020-03-02$$n14$$p2943-2959$$tThe Journal of Neuroscience$$v40$$x0270-6474$$y2020
000151528 773__ $$0PERI:(DE-600)1475274-8$$a10.1523/JNEUROSCI.2316-19.2020$$gVol. 40, no. 14, p. 2943 - 2959$$n14$$p2943-2959$$tThe journal of neuroscience$$v40$$x0270-6474$$y2020
000151528 8564_ $$uhttps://www.jneurosci.org/content/40/14/2943.abstract
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