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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, Patrick ; Moreno, H ; Khan, U. ; Vörckel, K. J. ; Wolfer, D. P. ; Welzl, H. ; Gall, D. ; Schiffmann, S. N. ; Schwaller, Beat

In: Translational Psychiatry, 2015, vol. 5, no. 3, p. e525

Gene mutations and gene copy number variants are associated with autism spectrum disorders (ASDs). Affected gene products are often part of signaling networks implicated in synapse formation and/or function leading to alterations in the excitation/inhibition (E/I) balance. Although the network of parvalbumin (PV)-expressing interneurons has gained particular attention in ASD, little is known on...