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1. Autistic-like behaviour in Scn1a +- mice and rescue by enhanced GABA-mediated neurotransmission

Author

Rubenstein, John, Han, S, Tai, C, Westenbroek, RE, Yu, FH, Cheah, CS, Potter, GB, Rubenstein, JL, Scheuer, T, De, HO, and Catterall, WA

Abstract

Haploinsufficiency of the SCN1A gene encoding voltage-gated sodium channel Na V 1.1 causes Dravets syndrome, a childhood neuropsychiatric disorder including recurrent intractable seizures, cognitive deficit and autism-spectrum behaviours. The neural mechan

Published
2012

2. List of Contributors

Author

Alvarenga, L.M., primary, Antunes, F., additional, Basso, A.M.M., additional, Billiald, P., additional, Callese, T., additional, Carvalho, K.A.T., additional, Castiglione, F., additional, Castilho, L.R., additional, Corrêa-Velloso, J.C., additional, Dalagostin, O., additional, de Cássia Oliveira Paiva, N., additional, Degrave, W.M.S., additional, Dellagostin, O.A., additional, de Medeiros, R.V.B., additional, de Moura, J., additional, Dias-Souza, M.V., additional, Edgar, L., additional, Felicori, L., additional, Felix, S.R., additional, Fendrich, R., additional, Gentile, C., additional, Gomes, A.Q., additional, Goulart, V.A.M., additional, Grossi-de-Sa, M.F., additional, Guedes, D., additional, Igel, D., additional, Jorge, S., additional, Katari, R., additional, Lima, H., additional, Marasco, D., additional, Marinho, H.S., additional, McNamara, K., additional, Mendes, T., additional, Mendonça-Lima, L., additional, Mondal, S., additional, Mor, A., additional, Nakamura, R., additional, Nardi Drummond, R.M., additional, Nascimento, I.C., additional, Ndoja, S., additional, Nery, A.A., additional, Nolasco, S., additional, Orlando, G., additional, Pandey, A., additional, Parreira, R.C., additional, Pelegrini, P.B., additional, Perottoni, C., additional, Pinto, M.C.X., additional, Prado, G.S., additional, Real, C., additional, Reddy, I.J., additional, Resende, R.R., additional, Sanson, R.K., additional, Santos, V.L., additional, Scheuer, T., additional, Severo, M.G., additional, Soares, H., additional, Soccol, C.R., additional, Souza, L.T., additional, Tamburrini, R., additional, Thomaz-Soccol, V., additional, Tieri, P., additional, Tonelli, F.C.P., additional, Tonelli, F.M.P., additional, Ulrich, H., additional, Vandenberghe, L.P.S., additional, Vitola, F., additional, Zambon, J.P., additional, and Zeferino, A.S., additional

Published
2017
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6. Reduction of cortical parvalbumin expressing GABAergic interneurons in a rodent hyperoxia model of preterm birth brain injury with deficits in social behavior and cognition

Author

Scheuer, T., Auf dem Brinke, E., Grosser, S., Wolf, S.A., Mattei, D., Sharkovska, Y., Barthel, P.C., Endesfelder, S., Friedrich, V., Bührer, C., Vida, I., and Schmitz, T.

Subjects
Function and Dysfunction of the Nervous System
Abstract

The inhibitory GABAergic system in the brain is involved in the etiology of various psychiatric problems, including autism spectrum disorders (ASD), attention deficit hyperactivity disorder (ADHD), and others. These disorders are influenced not only by genetic but also by environmental factors, such as preterm birth, although the mechanisms underlying are not known. In a translational hyperoxia model, exposing mice pups at age P5 to 80% oxygen for 48 hours to mimic a steep rise of oxygen exposure caused by preterm birth from in utero into room air, we documented a persistent reduction of cortical mature parvalbumin expressing interneurons until adulthood. Developmental delay of cortical myelin was observed together with decreased expression of oligodendroglial glial cell-derived neurotrophic factor (GDNF), a factor being involved in interneuronal development. Electrophysiological and morphological properties of remaining interneurons were unaffected. Behavioral deficits were observed for social interaction, learning, and attention. These results elucidate that neonatal oxidative stress can lead to decreased interneuron density and to psychiatric symptoms. The obtained cortical myelin deficit and decreased oligodendroglial GDNF expression indicate an impaired oligodendroglial-interneuronal interplay contributes to interneuronal damage.

Published
2021

10. Structure and function of the beta-2 subunit of brain sodium channels, a transmembrane glycoprotein with a CAM motif

Author

Isom, L.L., Ragsdale, D.S., De Jongh, K.S., Westenbroek, R.E., Reber, B.F.X., Scheuer, T., and Catterall, W.A.

Subjects
Sodium channels -- Research, Cloning -- Observations, Amino acid sequence -- Analysis, Biological sciences
Abstract

The beta-2 subunits of voltage-gated sodium channels play a major role in the regulation of sodium channel expression in neurons. A study of cDNA cloning and sequencing of the beta-2 subunit indicates the presence of a 186 residue glycoprotein with an extracellular NH2-terminal region. The region has an immunoglobulin-like fold, with resemblance to contactin, a small intracellular domain and a single transmembrane segment.

Published
1995

14. Association of rare missense variants in the second intracellular loop of NaV1.7 sodium channels with familial autism

Author

Rubinstein, M, primary, Patowary, A, additional, Stanaway, I B, additional, McCord, E, additional, Nesbitt, R R, additional, Archer, M, additional, Scheuer, T, additional, Nickerson, D, additional, Raskind, W H, additional, Wijsman, E M, additional, Bernier, R, additional, Catterall, W A, additional, and Brkanac, Z, additional

Published
2016
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22. Association of rare missense variants in the second intracellular loop of NaV1.7 sodium channels with familial autism

Author

Rubinstein, M, Patowary, A, Stanaway, I B, McCord, E, Nesbitt, R R, Archer, M, Scheuer, T, Nickerson, D, Raskind, W H, Wijsman, E M, Bernier, R, Catterall, W A, and Brkanac, Z

Abstract

Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder often accompanied by intellectual disability, language impairment and medical co-morbidities. The heritability of autism is high and multiple genes have been implicated as causal. However, most of these genes have been identified in de novo cases. To further the understanding of familial autism, we performed whole-exome sequencing on five families in which second- and third-degree relatives were affected. By focusing on novel and protein-altering variants, we identified a small set of candidate genes. Among these, a novel private missense C1143F variant in the second intracellular loop of the voltage-gated sodium channel NaV1.7, encoded by the SCN9A gene, was identified in one family. Through electrophysiological analysis, we show that NaV1.7C1143Fexhibits partial loss-of-function effects, resulting in slower recovery from inactivation and decreased excitability in cultured cortical neurons. Furthermore, for the same intracellular loop of NaV1.7, we found an excess of rare variants in a case–control variant-burden study. Functional analysis of one of these variants, M932L/V991L, also demonstrated reduced firing in cortical neurons. However, although this variant is rare in Caucasians, it is frequent in Latino population, suggesting that genetic background can alter its effects on phenotype. Although the involvement of the SCN1A and SCN2A genes encoding NaV1.1 and NaV1.2 channels in de novo ASD has previously been demonstrated, our study indicates the involvement of inherited SCN9A variants and partial loss-of-function of NaV1.7 channels in the etiology of rare familial ASD.

Published
2018
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28. Rollstuhlsport

Author

Scheuer, T., primary, Anneken, V., additional, Richarz, P., additional, Hirschfeld, S., additional, Hanssen-Doose, A., additional, and Thietje, R., additional

Published
2010
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