Cells were retrospectively immunolabeled for MAP-2, to distinguish axons from dendrites (data not shown).
EGFP-expressing cells in these damaged areas showed abnormal morphology, including pathological swellings and thick dendrites (data not shown).
In most cases, as the dendritic thickness in the proximal dendrite was larger than in the distal dendrite (data not shown), the number of synapses in the proximal dendrite was also larger than the distal dendrite (Fig. 3B).
Labeled mitral cells, which project to higher brain centers, exhibited typical MOB morphology: they displayed extensive lateral dendrites and a single apical dendrite (data not shown).
By contrast, spine density in tertiary basal dendrite branches did not significantly change after the injury; F 2, 33) = 2.035, P = 0.217).
Basal dendrites from transgenic neurons did not show differences in total dendritic spines as compared to WT.
NMDAR KO pyramidal cells displayed a decreased total spine density in the apical dendrites but not the basal dendrites (apical GFP: 2.63 ± 0.12, n = 38 frames, cre: 2.12 ± 0.17, n = 15 frames, p = 0.023, basal GFP: 2.59 ± 0.11, n = 28 frames, cre: 2.44 ± 0.15, n = 15 frames, p = 0.44; Figure 6C).
along all basal dendrites considered in the model (BLACK motion).
Moreover, Epotris affected the number of persistent basal dendrites exhibited by neuronal progenitor cells.
Seizure-induced hilar basal dendrites on dentate granule cells are observed in several rodent models of temporal lobe epilepsy.
