Enhanced LTP of population spikes in the dentate gyrus of mice haploinsufficient for neurobeachin.

Muellerleile, Julia; Blistein, Aline; Rohlmann, Astrid; Scheiwe, Frederieke; Missler, Markus; Schwarzacher, Stephan W; Jedlicka, Peter

Muellerleile, Julia; Blistein, Aline; Rohlmann, Astrid; Scheiwe, Frederieke; Missler, Markus; Schwarzacher, Stephan W; Jedlicka, Peter.

Afiliación

Muellerleile J; Institute of Clinical Neuroanatomy, Neuroscience Center, Goethe University Frankfurt am Main, Frankfurt, Germany. muellerleile@med.uni-frankfurt.de.
Blistein A; Faculty of Biosciences, Goethe University Frankfurt am Main, Frankfurt, Germany. muellerleile@med.uni-frankfurt.de.
Rohlmann A; Institute of Clinical Neuroanatomy, Neuroscience Center, Goethe University Frankfurt am Main, Frankfurt, Germany. aline_blistein@web.de.
Scheiwe F; Institute of Anatomy and Molecular Neurobiology, University of Münster, Münster, Germany.
Missler M; Institute of Anatomy and Molecular Neurobiology, University of Münster, Münster, Germany.
Schwarzacher SW; Institute of Anatomy and Molecular Neurobiology, University of Münster, Münster, Germany.
Jedlicka P; Institute of Clinical Neuroanatomy, Neuroscience Center, Goethe University Frankfurt am Main, Frankfurt, Germany.

Sci Rep ; 10(1): 16058, 2020 09 29.

Article en En | MEDLINE | ID: mdl-32994505

RESUMEN

Deletion of the autism candidate molecule neurobeachin (Nbea), a large PH-BEACH-domain containing neuronal protein, has been shown to affect synaptic function by interfering with neurotransmitter receptor targeting and dendritic spine formation. Previous analysis of mice lacking one allele of the Nbea gene identified impaired spatial learning and memory in addition to altered autism-related behaviours. However, no functional data from living heterozygous Nbea mice (Nbea+/-) are available to corroborate the behavioural phenotype. Here, we explored the consequences of Nbea haploinsufficiency on excitation/inhibition balance and synaptic plasticity in the intact hippocampal dentate gyrus of Nbea+/- animals in vivo by electrophysiological recordings. Based on field potential recordings, we show that Nbea+/- mice display enhanced LTP of the granule cell population spike, but no differences in basal synaptic transmission, synapse numbers, short-term plasticity, or network inhibition. These data indicate that Nbea haploinsufficiency causes remarkably specific alterations to granule cell excitability in vivo, which may contribute to the behavioural abnormalities in Nbea+/- mice and to related symptoms in patients.

Asunto(s)

Proteínas Portadoras/genética; Proteínas Portadoras/metabolismo; Potenciación a Largo Plazo/genética; Proteínas del Tejido Nervioso/genética; Proteínas del Tejido Nervioso/metabolismo; Animales; Trastorno del Espectro Autista/genética; Trastorno Autístico/genética; Encéfalo/metabolismo; Espinas Dendríticas/genética; Espinas Dendríticas/fisiología; Giro Dentado/metabolismo; Haploinsuficiencia; Hipocampo/metabolismo; Humanos; Masculino; Proteínas de la Membrana/metabolismo; Memoria; Ratones; Ratones Endogámicos C57BL; Ratones Transgénicos; Plasticidad Neuronal/genética; Neuronas/metabolismo; Sinapsis/metabolismo; Transmisión Sináptica/genética

Texto completo

Añadir a Mi BVS

Imprimir

XML

PubMed Links

Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Proteínas Portadoras / Potenciación a Largo Plazo / Proteínas del Tejido Nervioso Límite: Animals / Humans / Male Idioma: En Revista: Sci Rep Año: 2020 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Reino Unido

Texto completo

Añadir a Mi BVS

Imprimir

XML

PubMed Links

Buscar en Google