Lack of parvalbumin in mice leads to behavioral deficits relevant to all human autism core symptoms and related neural morphofunctional abnormalities

Wöhr, M, Orduz, D, Gregory, P, Moreno, H, Khan, U, Vörckel, K J, Wolfer, D P, Welzl, H +3 more·2015·Translational Psychiatry
DOI 10.1038/tp.2015.19

Cited by (257)

Items 201–257 of 257

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  41. Additional file 1 of Absence of parvalbumin increases mitochondria volume and branching of dendrites in inhibitory Pvalb neurons in vivo: a point of convergence of autism spectrum disorder (ASD) risk gene phenotypes
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  43. Additional file 1 of Maternal immunoglobulin G affects brain development of mouse offspring
    Mizuki Sadakata, Kazuki Fujii, Kaneko, Ryosuke, Emi Hosoya, Sugimoto, Hisako, Reika Kawabata‐Iwakawa, Tetsuhiro Kasamatsu, Shoko Hongo, Koshidaka, Yumie, Takase, Akinori et al. · 2024 · Figshare
  44. Additional file 1 of Shank3 deletion in PV neurons is associated with abnormal behaviors and neuronal functions that are rescued by increasing GABAergic signaling
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  45. Additional file 2 of Characterization of an eutherian gene cluster generated after transposon domestication identifies Bex3 as relevant for advanced neurological functions
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  52. Hypoactivity, abnormal development of dendrites relevant to impaired synaptic transmission of calretinin-expressing interneurons in the medial prefrontal cortex underlies social deficits of mouse model in autism
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