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This review evaluates changes in spine density and dendritic arborization in animal models of schizophrenia.
i, Relative changes in spine density on apical dendrites (cortical layer 2/3) measured by confocal microscopy in brain slices of rats transferred with the indicated antigen-specific T cells.
Overall, the changes in spine density together with the reduction in mEPSC frequency, demonstrate a deficit in excitatory neurotransmission in the mPFC of GluN2C KO that occurs early during development.
This delay in glutamatergic synaptogenesis was paralleled by a decrease in dendritic length with no changes in spine density, consistent with a protracted dendritic development without alterations in synapse formation.
These changes in spine density were accompanied by altered expression of proteins known to interact with PSD-95, including NR2B and SAP102, suggesting that PSD-95 plays a role in regulating the expression and activation of proteins found within the NMDA receptor complex.
No significant changes in spine density were detected for the basal dendrites (Figure 1F and H).
Similar(39)
Jones et al. [38] also noted that changes in spine densities are observed in patients with schizophrenia.
Moreover, in the proximal dendrites of PCs that expressed GluRδ2, we observed a marked change in spine density and CF varicosity distribution.
The increase in dendritic spine density concomitant with an overall increase in dendritic length and branching suggests that the change in spine density reflects an overall increase in spine number, rather than an increase in spine density due to dendrite shrinkage.
Using STED microscopy we found no change in spine density at a similar age (P37) in mice (7).
Moreover, there was no detectable change in spine density in medial prefrontal cortex or anterior cingulate cortex of the cKO mice.
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