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Molecular evidence for decreased synaptic efficacy in the postmortem olfactory bulb of individuals with schizophrenia

journal contribution
posted on 2023-05-20, 00:32 authored by Egbujo, CN, Duncan SinclairDuncan Sinclair, Borgmann-Winter, KE, Arnold, SE, Turetsky, BI, Hahn, C-G
Multiple lines of evidence suggest altered synaptic plasticity/connectivity as a pathophysiologic mechanism for various symptom domains of schizophrenia. Olfactory dysfunction, an endophenotype of schizophrenia, reflects altered activity of the olfactory circuitry, which conveys signals from olfactory receptor neurons to the olfactory cortex via synaptic connections in the glomeruli of the olfactory bulb. The olfactory system begins with intranasal olfactory receptor neuron axons synapsing with mitral and tufted cells in the glomeruli of the olfactory bulb, which then convey signals directly to the olfactory cortex. We hypothesized that olfactory dysfunction in schizophrenia is associated with dysregulation of synaptic efficacy in the glomeruli of the olfactory bulb. To test this, we employed semi-quantitative immunohistochemistry to examine the olfactory bulbs of 13 postmortem samples from schizophrenia and their matched control pairs for glomerular expression of 5 pre- and postsynaptic proteins that are involved in the integrity and function of synapses. In the glomeruli of schizophrenia cases compared to their matched controls, we found significant decreases in three presynaptic proteins which play crucial roles in vesicular glutamate transport - synapsin IIa (-18.05%, p=0.019), synaptophysin (-24.08% p=0.0016) and SNAP-25 (-23.9%, p=0.046). Two postsynaptic proteins important for spine formation and glutamatergic signaling were also decreased-spinophilin (-17.40%, p=0.042) and PSD-95 (-34.06%, p=0.015). These findings provide molecular evidence for decreased efficacy of synapses within the olfactory bulb, which may represent a synaptic mechanism underlying olfactory dysfunction in schizophrenia.

History

Publication title

Schizophrenia Research

Volume

168

Issue

1-2

Pagination

554-562

ISSN

0920-9964

Department/School

Wicking Dementia Research Education Centre

Publisher

Elsevier Science Bv

Place of publication

Po Box 211, Amsterdam, Netherlands, 1000 Ae

Rights statement

Copyright 2015 Elsevier B.V.

Repository Status

  • Restricted

Socio-economic Objectives

Clinical health not elsewhere classified

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