Normal cellular levels of synaptophysin mRNA expression in the prefrontal cortex of subjects with schizophrenia

Glantz, Leisa A.; Austin, Mark C.; Lewis, David A.

doi:10.1016/s0006-3223(00)00923-9

Cited by 64 publications

(42 citation statements)

References 42 publications

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“…27 No differences between schizophrenics and controls were detected in three investigations of synaptophysin mRNA in the PFC. 26,27,58 Synaptophysin mRNA was also measured, using in situ hybridization, in a subset of subjects from the cohort examined in our current study, and no difference between the groups was found (Weickert et al, unpublished observations). In summary, these findings suggest that synaptophysin mRNA expression is most likely unaffected in schizophrenia, whereas the protein levels may be reduced in certain subgroups of patients, although perhaps not the majority.…”

Section: Discussionmentioning

confidence: 62%

Presynaptic proteins in the prefrontal cortex of patients with schizophrenia and rats with abnormal prefrontal development

et al. 2003

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Section: Discussionmentioning

confidence: 62%

Presynaptic proteins in the prefrontal cortex of patients with schizophrenia and rats with abnormal prefrontal development

et al. 2003

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“…In line with this is the finding of reduced spines on the pyramidal neurons, in both the prefrontal and temporal cortex, 45,46 since the spines generally correspond to synaptic sites. Evidence of abnormal synaptic profiles (for recent data on temporal cortex and references, see Ong and Garey 47 ) and decreased concentration of synaptic proteins, [48][49][50] in the absence of RNA or mRNA decrease, 51 similarly suggest loss of synaptic boutons. However, dysregulation of several presynaptic proteins, including synapsin II, might also occur independent of synaptic elimination.…”

Section: Connectivism and Schizophreniamentioning

confidence: 99%

Schizophrenia, neurodevelopment and corpus callosum

2003

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The Zeitgeist favors an interpretation of schizophrenia as a condition of abnormal connectivity of cortical neurons, particularly in the prefrontal and temporal cortex. The available evidence points to reduced connectivity, a possible consequence of excessive synaptic pruning in development. A decreased thalamic input to the cerebral cortex appears likely, and developmental studies predict that this decrease should entail a secondary loss of both longand short-range cortico-cortical connections, including connections between the hemispheres. Indeed, morphological, electrophysiological and neuropsychological studies over the last two decades suggest that the callosal connections are altered in schizophrenics. However, the alterations are subtle and sometimes inconsistent across studies, and need to be investigated further with new methodologies.

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“…Conversely, aberrant synaptophysin expression has been associated with several neurodegenerative diseases and psychiatric disorders, such as Alzheimer's disease and schizophrenia (20 -24). In some cases, an alteration in the protein level of synaptophysin is observed without a concomitant change at the mRNA level (22), implying that impaired post-translational regulation may contribute to abnormal synaptophysin expression.…”

mentioning

confidence: 99%

Regulation of Synaptophysin Degradation by Mammalian Homologues of Seven in Absentia

Wheeler

Chin

et al. 2002

Journal of Biological Chemistry

148

134

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Synaptophysin is an integral membrane protein of synaptic vesicles characterized by four transmembrane domains with both termini facing the cytoplasm. Although synaptophysin has been implicated in neurotransmitter release, and decreased synaptophysin levels have been associated with several neurodegenerative diseases, the molecular mechanism that regulates the degradation of synaptophysin remains unsolved. Using the cytoplasmic C terminus of synaptophysin as bait in a yeast two-hybrid screen, we identified two synaptophysin-binding proteins, Siah-1A and Siah-2, which are rat homologues of Drosophila Seven in Absentia. We demonstrated that Siah-1A and Siah-2 associate with synaptophysin both in vitro and in vivo and defined the binding domains of synaptophysin and Siah that mediate their association. Siah proteins exist in both cytosolic and membrane-associated pools and co-localize with synaptophysin on synaptic vesicles and early endosomes. In addition, Siah proteins interact specifically with the brain-enriched E2 ubiquitin-conjugating enzyme UbcH8 and facilitate the ubiquitination of synaptophysin. Furthermore, overexpression of Siah proteins promotes the degradation of synaptophysin via the ubiquitin-proteasome pathway. Our findings indicate that Siah proteins function as E3 ubiquitin-protein ligases to regulate the ubiquitination and degradation of synaptophysin.

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Normal cellular levels of synaptophysin mRNA expression in the prefrontal cortex of subjects with schizophrenia

Cited by 64 publications

References 42 publications

Presynaptic proteins in the prefrontal cortex of patients with schizophrenia and rats with abnormal prefrontal development

Presynaptic proteins in the prefrontal cortex of patients with schizophrenia and rats with abnormal prefrontal development

Schizophrenia, neurodevelopment and corpus callosum

Regulation of Synaptophysin Degradation by Mammalian Homologues of Seven in Absentia

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