Syndapin I Loss-of-Function in Mice Leads to Schizophrenia-Like Symptoms.

Cerebral Cortex
Nicole KochBritta Qualmann

Abstract

Schizophrenia is associated with cognitive and behavioral dysfunctions thought to reflect imbalances in neurotransmission systems. Recent screenings suggested that lack of (functional) syndapin I (PACSIN1) may be linked to schizophrenia. We therefore studied syndapin I KO mice to address the suggested causal relationship to schizophrenia and to analyze associated molecular, cellular, and neurophysiological defects. Syndapin I knockout (KO) mice developed schizophrenia-related behaviors, such as hyperactivity, reduced anxiety, reduced response to social novelty, and an exaggerated novel object response and exhibited defects in dendritic arborization in the cortex. Neuromorphogenic deficits were also observed for a schizophrenia-associated syndapin I mutant in cultured neurons and coincided with a lack of syndapin I-mediated membrane recruitment of cytoskeletal effectors. Syndapin I KO furthermore caused glutamatergic hypofunctions. Syndapin I regulated both AMPAR and NMDAR availabilities at synapses during basal synaptic activity and during synaptic plasticity-particularly striking were a complete lack of long-term potentiation and defects in long-term depression in syndapin I KO mice. These synaptic plasticity defects coincided...Continue Reading

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Citations

Jun 5, 2020·Cells·Jessica TrögerPeter Hemmerich
Sep 15, 2020·Current Opinion in Cell Biology·Michael M Kessels, Britta Qualmann
Aug 24, 2021·Frontiers in Molecular Biosciences·Zhou ZimuShan Enfang

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