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1 stinctive activity-dependent critical period dendritic remodeling.
2 1) signaling in stress-evoked spine loss and dendritic remodeling.
3 o-mediated signaling is sufficient to induce dendritic remodeling.
4 of Ca(2+) spikes may influence postembryonic dendritic remodeling.
5 o show normal synaptic responses and undergo dendritic remodeling.
6 be important for rapid, compartment-specific dendritic remodeling.
10 BA(A) receptor system may also contribute to dendritic remodeling and other stress-related changes in
11 dent stress and depression models have found dendritic remodeling and synaptic spines reduction in co
12 ssion in hSOD1(G93A) HMs revealed precocious dendritic remodeling, and behavioral assays revealed tra
13 hyperglycemia and prevention of hippocampal dendritic remodeling, and therefore, provides an effecti
14 s; spontaneous activity-dependent axonal and dendritic remodeling; and sensory-evoked plasticity driv
15 These increases were followed by a period of dendritic remodeling during which the values for all mea
16 tigation was to improve our understanding of dendritic remodeling exhibited by second-order gustatory
17 These results suggest that Purkinje neuron dendritic remodeling in ataxia is an adaptive response t
20 f neurogenesis in the dentate gyrus (DG) and dendritic remodeling in the cornu ammonis (CA), particul
21 res the current literature on stress-induced dendritic remodeling in the mPFC, with particular focus
22 tudy provides the first direct evidence that dendritic remodeling in the prefrontal cortex may underl
24 GLT-1 protein levels in the subregion where dendritic remodeling is most prominent, namely the CA3 r
25 or both of these neurotrophins in axonal and dendritic remodeling known to accompany the formation of
31 microtubule-associated protein-2 may reflect dendritic remodeling related to contextual memory storag
33 s emerge as novel mediators of BDNF-mediated dendritic remodeling through the activation of a slowly
34 ressant tianeptine, which blocks CRS-induced dendritic remodeling, to modulate CRS-mediated changes i
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