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The possibly reduced spine size may lead to the decreased responses of single synaptic event.
Changes in dendritic spine size accompany synapse maturation [1] and are correlated with synaptic strength [2] [4].
It should be noted that the dominant negative Rac3 construct did not reduce dendritic spine size compared to control cells.
Spine size was normal in cells co-expressing a dominant negative Rac3 construct with the βI-spectrin ABD.
We also show here that TRIM3 negatively regulates the size of spine heads, with loss of function resulting in increased spine size.
Shank1b promotes maturation of dendritic spines [19], while its dominant negative mutant causes a reduction in spine size and density [20].
In this instance no fission was observed (Fig. 7A C) although neuronal morphology was altered with blebbing of dendrites and reduced spine size.
Similarly, genetic deletion of Rac3 does not affect dendritic spine density in hippocampal cell cultures [75], although spine size was not quantified.
However, in organotypic hippocampal slices, electron microscope (EM) 3D reconstruction, revealed no changes of the overall spine size 2 hours post-tetanus [49].
Within minutes there are increases in spine size [18], [19], clusters or puncta of both postsynaptic glutamate receptors [20] and presynaptic vesicle-associated proteins, as well as sites where the pre- and postsynaptic puncta colocalize [21], [22].
PICK1 knockdown increases spine size, whereas PICK1 overexpression reduces spine size.
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