Impaired synaptic plasticity in an animal model of autism exhibiting early hippocampal GABAergic-BDNF/TrkB signaling alterations
Martina Sgritta, Beatrice Vignoli, Domenico Pimpinella, Marilena Griguoli, Spartaco Santi, Andrzej Bialowas, Grzegorz Wiera, Paola Zacchi, Francesca Malerba, Cristina Marchetti, Marco Canossa, Enrico Cherubini
Abstract
gene (NLG3 KO mice), suggesting a loss of function. The loss of STD-LTP was associated with a premature shift of GABA from the depolarizing to the hyperpolarizing direction, a reduced BDNF availability and TrkB phosphorylation at potentiated synapses. These effects may constitute a general mechanism underlying cognitive deficits in those forms of Autism caused by synaptic dysfunctions.
Topics & Concepts
NeuroscienceGlutamatergicSynaptic plasticityTropomyosin receptor kinase BLong-term potentiationHippocampal formationGABAergicMetaplasticityNeuroplasticityHippocampusAutismBiologyPsychologyNeurotrophic factorsGlutamate receptorInhibitory postsynaptic potentialPsychiatryGeneticsReceptorNeuroscience and Neuropharmacology ResearchNerve injury and regenerationRNA Interference and Gene Delivery