Characterization of olfactory bulb glomeruli in schizophrenia

Rioux, Lise; Gelber, Edward I.; Parand, Leila; Kazi, Hala; Yeh, Joannie T.; Wintering, Rebecca; Bilker, Warren B.; Arnold, Steven E.

doi:10.1016/j.schres.2005.04.022

Cited by 10 publications

(8 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, the OE establishes synaptic connections with the OB to obtain trophic support, presumably there may be an undefined difficulty in establishing healthy synaptic connections with the abnormal OB in CUMS rats, which may be due to ORNs decreasing. This would go along with a previous study showing that ORNs proliferation was significantly decreased in the OE of rat which underwent olfactory bulbectomy [10,13,37]. Taken together, the exact reason of the decrease of ORNs in CUMS rat requests further research.…”

Section: Discussionsupporting

confidence: 70%

Reduced amount of olfactory receptor neurons in the rat model of depression

Yang

Wang

et al. 2015

Neuroscience Letters

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 70%

Reduced amount of olfactory receptor neurons in the rat model of depression

Yang

Wang

et al. 2015

Neuroscience Letters

View full text Add to dashboard Cite

“…b-Tubulin has previously been used as internal control 52,53 and several studies have found expression of b-Tubulin to be unaffected in schizophrenic brain. 54,55 However, in order to further minimize the potential effect of dendritic loss on bTubulin expression, we used an antibody that recognizes not only the neuron-specific isoform III, but all b-Tubulin isoforms (I, II, III, IVa and IVb), representing both neuronal and non-neuronal tubulin expression. Examples of representative immunoblots are shown in Figure 1a.…”

Section: Resultsmentioning

confidence: 99%

Changes in NMDA receptor subunits and interacting PSD proteins in dorsolateral prefrontal and anterior cingulate cortex indicate abnormal regional expression in schizophrenia

et al. 2006

View full text Add to dashboard Cite

Abnormal expression of the N-Methyl-D-Aspartate (NMDA) receptor and its interacting molecules of the postsynaptic density (PSD) are thought to be involved in the pathophysiology of schizophrenia. Frontal regions of neocortex including dorsolateral prefrontal (DLPFC) and anterior cingulate cortex (ACC) are essential for cognitive and behavioral functions that are affected in schizophrenia. In this study, we have measured protein expression of two alternatively spliced isoforms of the NR1 subunit (NR1 C2 and NR1 C2 0 ) as well as expression of the NR2A-D subunits of the NMDA receptor in DLPFC and ACC in post-mortem samples from elderly schizophrenic patients and a comparison group. We found significantly increased expression of NR1 C2 0 but not of NR1 C2 in ACC, suggesting altered NMDA receptor cell membrane expression in this cortical area. We did not find significant changes in the expression of either of the NR1 isoforms in DLPFC. We did not detect changes of any of the NR2 subunits studied in either cortical area. In addition, we studied expression of the NMDAinteracting PSD molecules NF-L, SAP102, PSD-95 and PSD-93 in ACC and DLPFC at both transcriptional and translational levels. We found significant changes in the expression of NF-L in DLPFC, and PSD-95 and PSD-93 in ACC; increased transcript expression was associated with decreased protein expression, suggesting abnormal translation and/or accelerated protein degradation of these molecules in schizophrenia. Our findings suggest abnormal regional processing of the NMDA receptor and its associated PSD molecules, possibly involving transcription, translation, trafficking and protein stability in cortical areas in schizophrenia.

show abstract

“…One study reported decreased MAP2 expression in OB glomeruli in schizophrenia (Rioux et al, 2004), suggesting a possible decrease in glomerular dendritic arborization which would be consistent with our findings. However, in a follow-up study, the same group did not identify differences in pre- and post-synaptic glomerular proteins OMP, GAP-43, NCAM, calbindin, NFM/HP, β-tubulin III or TrkB, and although synaptophysin was decreased by about 13% it was not statistically significant (Rioux et al, 2005). Further work is required to determine to what extent pre- and postsynaptic deficits in OB glomeruli are a consistent feature of schizophrenia, and to clarify whether deficits are specific to key cellular processes such as vesicular transport, which was the predominant focus of this study.…”

Section: Discussionmentioning

confidence: 98%

“…Glomeruli were readily identified as areas of increased density of pre- and post-synaptic protein immunostaining within the glomerular layer of the bulb. The gray value for each glomerulus within each section was recorded and converted to an OD value, from which was subtracted the background OD (obtained from non-stained portion of the bulb), yielding the mean OD of each protein across all glomeruli in the section (Balu et al, 2012; Rioux et al, 2005; Talbot et al, 2004). All background-corrected mean glomerular OD data were approximately normally distributed (skewness between −1 and 1).…”

Section: Methodsmentioning

confidence: 99%

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

Egbujo

Sinclair

Borgmann‐Winter

et al. 2015

Schizophrenia Research

View full text Add to dashboard Cite

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.

show abstract

Characterization of olfactory bulb glomeruli in schizophrenia

Cited by 10 publications

References 63 publications

Reduced amount of olfactory receptor neurons in the rat model of depression

Reduced amount of olfactory receptor neurons in the rat model of depression

Changes in NMDA receptor subunits and interacting PSD proteins in dorsolateral prefrontal and anterior cingulate cortex indicate abnormal regional expression in schizophrenia

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

Contact Info

Product

Resources

About