Glutamatergic dysfunction and synaptic ultrastructural alterations in 
schizophrenia and autism spectrum disorder: evidence from human and rodent 
studies

Eltokhi, Ahmed; Santuy, Andrea; Merchan-Perez, Angel; Sprengel, Rolf

doi:10.3390/ijms22010059

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Glutamatergic dysfunction and synaptic ultrastructural alterations in schizophrenia and autism spectrum disorder: evidence from human and rodent studies

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Sprengel, Rolf
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Eltokhi, A., Santuy, A., Merchan-Perez, A., & Sprengel, R. (2020). Glutamatergic dysfunction and synaptic ultrastructural alterations in schizophrenia and autism spectrum disorder: evidence from human and rodent studies. International Journal of Molecular Sciences, 22(1): 59, pp. 1-26. doi:10.3390/ijms22010059.

Cite as: https://hdl.handle.net/21.11116/0000-0007-A5B9-E

Abstract

The correlation between dysfunction in the glutamatergic system and neuropsychiatric disorders, including schizophrenia and autism spectrum disorder, is undisputed. Both disorders are associated with molecular and ultrastructural alterations that affect synaptic plasticity and thus the molecular and physiological basis of learning and memory. Altered synaptic plasticity, accompanied by changes in protein synthesis and trafficking of postsynaptic proteins, as well as structural modifications of excitatory synapses, are critically involved in the postnatal development of the mammalian nervous system. In this review, we summarize glutamatergic alterations and ultrastructural changes in synapses in schizophrenia and autism spectrum disorder of genetic or drug-related origin, and briefly comment on the possible reversibility of these neuropsychiatric disorders in the light of findings in regular synaptic physiology