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1 ebrin A more strongly than spines containing drebrin A.
2 and areal density of spine profiles lacking drebrin A.
4 ment in the proportion of spines labeled for drebrin A and no significant change in spine density at
6 overed two domains in the N-terminal half of drebrin-a coiled-coil domain and a helical domain-that i
8 nts confirmed that the reduced proportion of drebrin A-containing spines in brains of FAD mice at 6 m
10 x of 2xKI mice, in which synapse density and drebrin A immunoreactivity levels remain unchanged at 6
13 nths and older, a larger fraction of spinous drebrin A in 2xKI mice was located near the synaptic mem
14 this end, a new antibody was used to locate drebrin A in relation to electron microscopically imaged
16 ght microscopy showed high concentrations of drebrin A in the synaptic layers of the hippocampus and
20 esumably excitatory) synapses and containing drebrin A is reduced and if so, whether this occurs prio
21 proportion of hippocampal spines containing drebrin A is reduced and this change is accompanied by a
23 In adulthood, nearly all of the synaptic drebrin A is within spines forming asymmetric excitatory
25 thood depends on an F-actin binding protein, drebrin A, mice deleted of the adult isoform of drebrin
26 s, soluble Abeta could affect spines lacking drebrin A more strongly than spines containing drebrin A
30 al density of postsynaptic spines containing drebrin A was relatively constant from 3 to 18 months an
32 , the proportion of postsynaptic spines with drebrin A within somatosensory cortex layer I was smalle
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