Impact of apoE deficiency during synaptic remodeling in the mouse olfactory bulb
Section snippets
Acknowledgements
This work was supported by National Institute on Deafness and Other Communication Disorder (DC 003889), Illinois Department of Public Health grant, and Eastern Illinois University CFR grants.
References (27)
- et al.
Effect of apolipoprotein E deficiency on reactive sprouting in the dentate gyrus of the hippocampus following entorhinal cortex lesion: role of the astroglial response
Exp. Neurol.
(2005) - et al.
Principles of organization of the vertebrate olfactory glomerulus: an hypothesis
Neuroscience
(1986) - et al.
Synaptophysin-like immunoreactivity in the rat olfactory bulb during postnatal development and after restricted early olfactory experience
Brain Res. Dev. Brain Res.
(1996) - et al.
Denervation in the primary olfactory pathway of mice: biochemical and morphological effects
Brain Res.
(1974) - et al.
Neurodegeneration in the central nervous system of apoE-deficient mice
Exp. Neurol.
(1995) - et al.
Alterations in apolipoprotein E expression during aging and neurodegeneration
Prog. Neurobiol.
(1996) - et al.
The distribution of apolipoprotein E in mouse olfactory epithelium
Brain Res.
(2007) - et al.
Apolipoprotein E is upregulated in olfactory bulb glia following peripheral receptor lesion in mice
Exp. Neurol.
(2001) - et al.
Delayed olfactory nerve regeneration in ApoE-deficient mice
Brain Res.
(2005) - et al.
192 IgG-saporin causes a major loss of synaptic content in rat olfactory bulb
Exp. Neurol.
(1994)
Parkinson's disease and apolipoprotein E: possible association with dementia but not age at onset
Genomics
Estradiol regulation of astroglia and apolipoprotein E: an important role in neuronal regeneration
Exp. Gerontol.
Apolipoprotein E immunoreactivity in human and mouse olfactory bulb
Neurosci. Lett.
Cited by (8)
Regulation of astroglia by gonadal steroid hormones under physiological and pathological conditions
2016, Progress in NeurobiologyCitation Excerpt :Another factor that may mediate estradiol-induced neuro-glial plasticity is apolipoprotein E (ApoE) (Struble et al., 2007), which levels have been shown to depend on gonadal steroid levels in vivo and in vitro (Stone et al., 1997; Struble et al., 2007). Although the precise mechanisms of ApoE in neuro-glial plasticity are still unknown, this molecule seems to be crucial for that function (Blain et al., 2006; Nwosu et al., 2008; White et al., 2001) and it is involved in the effects of estradiol on axonal growth in vitro (Nathan et al., 2004). As in the arcuate nucleus, estradiol and progesterone also induce plastic remodeling of astrocytes in the hippocampus.
At the interface of sensory and motor dysfunctions and Alzheimer's disease
2015, Alzheimer's and DementiaLong-term effects of estradiol replacement in the olfactory system
2012, Experimental NeurologyCitation Excerpt :Our study started 5 days following OVX at which time we found no difference between genotypes for CV, OMP or GFAP. Syn was less in the apoE KO as we and others have previously reported (Masliah et al., 1995; Nwosu et al., 2008). We then implanted estradiol or vehicle and started sampling treated groups at 3 days (8 days post OVX).
Acute responses to estradiol replacement in the olfactory system of apoE-deficient and wild-type mice
2010, Brain ResearchCitation Excerpt :GFAP+ processes were counted by placing a 5 × 5 grid box over the digital image, and astrocyte processes were marked with a dot if they crossed the grid (Struble et al., 2006). Syn quantification was performed as described (Nwosu et al., 2008). All quantification procedures were performed using three mice per genotype (WTand KO) and three mice per treatment (estrogen and vehicle).
Genetic influences on neural plasticity
2010, PM and RCitation Excerpt :Studies in animal models and cell culture suggest that ApoE is also important in CNS plasticity. Levels of the ApoE protein spontaneously increase after olfactory bulb lesion [126], and ApoE knockout mice show delayed and diminished synaptic recovery after olfactory bulb lesions compared with wild-type mice [127]. Recent evidence has shown that ApoE4 results in less NMDA receptor activation in response to Reelin signaling, a potential mechanism for its affect on synaptic plasticity [128].
- 1
These authors contributed equally to this study.