Shank3 transgenic and prenatal zinc-deficient autism mouse models show convergent and Individual alterations of brain structures in MRI
Wissenschaftlicher Artikel
Authors
Schön, Michael
Asoglu, Harun
Bauer, Helen F.
Müller, Hans-Peter
Abaei, Alireza
Faculties
Medizinische FakultätInstitutions
Institut für Anatomie und ZellbiologieZentrum für Translationale Bildgebung (MoMan)
External cooperations
Peking UniversityNational Health and Family Planning Commission of the People's Republic of China
University of Limerick
Published in
Frontiers in Neural Circuits ; 13 (2019). - Art.-Nr. 6. - eISSN 1662-5110
Link to original publication
https://dx.doi.org/10.3389/fncir.2019.00006Peer review
ja
Document version
publishedVersion
Abstract
Research efforts over the past decades have unraveled both genetic and environmental factors, which contribute to the development of autism spectrum disorders (ASD). It is, to date, largely unknown how different underlying causes result in a common phenotype. However, the individual course of development and the different comorbidities might reflect the heterogeneous genetic and non-genetic contributions. Therefore, it is reasonable to identify commonalities and differences in models of these disorders at the different hierarchical levels of brain function, including genetics/environment, cellular/synaptic functions, brain regions, connectivity, and behavior. To that end, we investigated Shank3 transgenic mouse lines and compared them with a prenatal zinc-deficient (PZD) mouse model of ASD at the level of brain structural alterations in an 11,7 T small animal magnetic resonance imaging (MRI). Animals were measured at 4 and 9 weeks of age. We identified a decreased total brain volume (TBV) and hippocampal size of Shank3-/- mice but a convergent increase of basal ganglia (striatum and globus pallidus) in most mouse lines. Moreover, Shank3 transgenic mice had smaller thalami, whereas PZD mice had this region enlarged. Intriguingly, Shank3 heterozygous knockout mice mostly showed minor abnormalities to full knockouts, which might reflect the importance of proper Shank3 dosage in neuronal cells. Most reported volume changes seemed to be more pronounced at younger age. Our results indicate both convergent and divergent brain region abnormalities in genetic and non-genetic models of ASD. These alterations of brain structures might be mirrored.
Funding information
Juniorprofessoren-Programm / Baden-Württemberg
BIU 2 / Universität Ulm
SFB 1149: Gefahrenantwort, Störfaktoren und regeneratives Potential nach akutem Trauma / DFG [251293561; SFB1149, A02]
RNA Dysmetabolism in ALS and FTD / Helmholtz Gesellschaft
Innovative Medicines Initiative (IMI) Joint [115300 ; 777394]
etc.
BIU 2 / Universität Ulm
SFB 1149: Gefahrenantwort, Störfaktoren und regeneratives Potential nach akutem Trauma / DFG [251293561; SFB1149, A02]
RNA Dysmetabolism in ALS and FTD / Helmholtz Gesellschaft
Innovative Medicines Initiative (IMI) Joint [115300 ; 777394]
etc.
Is supplemented by
https://www.frontiersin.org/articles/10.3389/fncir. 2019.00006/full#supplementary-materialSubject Headings
Autismus [GND]Tiermodell [GND]
Zinkmangel [GND]
Kernspintomografie [GND]
Autism spectrum disorder [MeSH]
Models, Animal [MeSH]
Zinc; Deficiency [MeSH]
Magnetic resonance imaging [MeSH]
Keywords
ASD; Autism mouse models; SHANK3; Brain structures; Animal MRIDewey Decimal Group
DDC 610 / Medicine & healthMetadata
Show full item recordCitation example
Schön, Michael et al. (2021): Shank3 transgenic and prenatal zinc-deficient autism mouse models show convergent and Individual alterations of brain structures in MRI. Open Access Repositorium der Universität Ulm. http://dx.doi.org/10.18725/OPARU-35135