Protective effects of osmolytes in cryopreserving adherent neuroblastoma (Neuro-2a) cells.

A simple method to cryopreserve adherent monolayers of neuronal cells is currently not available, but the development of this technique could facilitate numerous applications in the field of biomedical engineering, cell line development, and drug screening. However, complex tissues of some exceptional animals survive freezing in nature. These animals are known to accumulate several small molecular weight solutes prior to freezing.

Neurite outgrowth promoting effect of 17-β estradiol is mediated through estrogen receptor alpha in an olfactory epithelium culture.

Olfactory deficits are observed early in the course of chronic neurological disorders including Alzheimer's disease (AD). Estrogen treatment in post-menopausal women reduced the incidence of olfactory dysfunction, raising the possibility that estrogen treatment can cure olfactory deficits in preclinical stages of AD. In this study, we examined the estradiol׳s effects on neurite outgrowth in explant cultures of mouse olfactory epithelium (OE).

Isoform-specific effects of apoE on neurite outgrowth in olfactory epithelium culture.

Background: The apolipoprotein E4 (apoE4) genotype is a major risk factor for developing late-onset Alzheimer's disease (AD). Inheritance of apoE4 is also associated with impairments in olfactory function in early stages of AD. In this project we examined the effects of the three common isoforms of human apoE (apoE2, apoE3, and apoE4) on neuronal differentiation and neurite outgrowth in explant cultures of mouse olfactory epithelium (OE).

Long-term effects of estradiol replacement in the olfactory system.

Olfactory dysfunction often precedes other clinical symptoms in chronic neurodegenerative diseases like Alzheimer's disease and Parkinson's disease. Estrogen deficiency and apoE genotype are known risk factors in these diseases and these factors also affect olfaction. Therefore we examined the effects of estradiol replacement following ovariectomy on expression of apoE and markers of cell proliferation, neuronal maturation, synaptogenesis and reactive gliosis in the primary olfactory pathway of wild-type (WT) and apoE knockout (KO) mice.

Reconstitution of the olfactory epithelium following injury in apoE-deficient mice.

ApoE, a protein component of lipoproteins, is extensively expressed in the primary olfactory pathway. Because apoE has been shown to play a vital role in nerve repair and remodeling, we hypothesized that apoE expression will increase in the injured olfactory epithelium (OE), and that apoE deficiency in apoE knockout (KO) mice will lead to delayed/incomplete reconstitution of the OE following injury. To directly test this hypothesis, we compared OE regeneration in wild-type (WT) and KO mice following injury induced by intranasal irrigation of Triton X-100.

Physiological status of male and female Popillia japonica (Coleoptera: Scarabaeidae) affects mating and grouping behavior.

Because mating may be costly, sexually active males or females are predicted to be in relatively good physiological condition and may preferentially direct their mating behavior toward relatively high-quality mates. We tested this hypothesis in Japanese beetles (Popillia japonica Newman), a pest species in which males and females may be either isolated or in aggregations while feeding on host plants. We examined male size and lipid content and female size and egg load with respect to both their pairing status and whether they were isolated or in aggregations.

Acute responses to estradiol replacement in the olfactory system of apoE-deficient and wild-type mice.

Epidemiological studies suggest that estrogen therapy protects against clinical expression of chronic neurological diseases. These beneficial effects of estrogen therapy are highly modified by apolipoprotein E (apoE) through an unknown mechanism. We examined the short-term effects of estradiol replacement in ovariectomized mice on apoE expression and markers for cell proliferation, reactive gliosis, neuronal maturation, and synaptogenesis in the primary olfactory pathway of wild-type (WT) and apoE knockout (KO) mice.

Impact of apoE deficiency during synaptic remodeling in the mouse olfactory bulb.

In this study we examined the role of apoE on the rate of synaptic recovery in the olfactory bulb (OB) following olfactory epithelium (OE) lesioning in mice. We used both immunoblotting and immunohistochemical techniques to compare the density of OB synaptophysin (Syn, a synaptic marker) in apoE-gene deficient/knockout (KO) mice and wild-type (WT) mice following OE lesion. We found that the whole bulb concentrations of Syn, measured by immunoblotting, declined sharply following injury in both WT and KO mice during the degenerative phase (3-7 days).

Apolipoprotein E may be a critical factor in hormone therapy neuroprotection.

In this review we examine the evidence for ovarian hormone neuroprotection in chronic neurological diseases, including stroke. We propose that neuroprotection may involve the ability of estrogens to modulate apolipoprotein E (apoE) and its receptor, the low density lipoprotein receptor related protein (LRP). Results from numerous studies have demonstrated that (1) nerve regeneration is severely delayed in apoE-gene knockout (KO) mice as compared to wild-type (WT) littermates; (2) 17beta estradiol replacement in ovariectomized mice resulted in a significant increase in levels of apoE and LRP, in the olfactory bulb (OB) and other brain areas; (3) estradiol treatment increased both apoE and neurite outgrowth in cortical and olfactory neuronal cultures; and (4) estradiol treatment had no effect on neurite outgrowth in cultures deprived of apoE or in the presence of apoE4.

Estradiol replacement increases the low-density lipoprotein receptor related protein (LRP) in the mouse brain.

Numerous epidemiology studies have shown protective effects of hormone therapy (HT) on chronic neurological diseases. We have proposed that some of the neuroprotective effects of estrogen are mediated by apolipoprotein E (apoE). Polymorphisms of receptors for apoE modify the risk for dementia.

The distribution of apolipoprotein E in mouse olfactory epithelium.

Previous studies from our laboratory suggest that apolipoprotein (apoE), a lipid transporting protein, facilitates olfactory nerve regeneration. We have shown that apoE is enriched in the olfactory nerve and around the glomeruli of the olfactory bulb (OB). The studies reported herein were undertaken to identify possible sources of apoE in the olfactory epithelium (OE).

Neocortical and hippocampal glial fibrillary acidic protein immunoreactivity shows region-specific variation during the mouse estrous cycle.

Ovarian hormones modulate both neuronal and glial activation during the estrous cycle. These effects are particularly well characterized in the hypothalamus. Ovarian hormones also affect brain regions not directly related to reproductive function.

Estradiol regulation of astroglia and apolipoprotein E: an important role in neuronal regeneration.

The effects of ovarian hormone on neuronal growth and function are well known. However, equally important, but often neglected, are ovarian hormone effects on glia. Our in vivo and in vitro studies show that estradiol modifies both neuronal growth and glial activity and these effects are tightly linked.

Time course of response to estradiol replacement in ovariectomized mice: brain apolipoprotein E and synaptophysin transiently increase and glial fibrillary acidic protein is suppressed.

The current study examined the effect of long-term estradiol replacement in ovariectomized mice. Estradiol-17beta (E2) pellets or vehicle pellets were implanted at the time of ovariectomy (OVX) in young adult female mice. Five mice from each group were sacrificed at 5, 14, 28 and 49 days after OVX and pellet replacement.

Delayed olfactory nerve regeneration in ApoE-deficient mice.

Apolipoprotein E (apoE), a lipid transporting protein, is extensively expressed in the primary olfactory pathway, but its function is unknown. We previously reported increased apoE levels in the olfactory bulb (OB) following olfactory epithelium (OE) lesion in mice, and hypothesized that apoE may play a vital role in olfactory nerve (ON) regeneration. To directly test this hypothesis, we examined the rate of ON regeneration following OE lesion in apoE deficient/knockout (KO) and wild-type (WT) mice.

Estrogen facilitates neurite extension via apolipoprotein E in cultured adult mouse cortical neurons.

Literature review suggests a close relationship between estrogen and apolipoprotein E (ApoE) in the central nervous system. Epidemiology studies show that estrogen replacement therapy (ERT) decreases the morbidity from several chronic neurological diseases. Alleles of ApoE modify the risk for and progression of the same diseases.

Olfactory function in apoE knockout mice.

Apolipoprotein E (apoE), a lipid transporting protein, has been shown to play a vital role in nerve repair and remodeling. Since the olfactory system is in a continuous state of remodeling, the present study tested the hypothesis that apoE is required for normal functioning of the olfactory system. Olfactory behavior of wild-type (WT) and apoE-deficient (apoE KO) mice was assessed by using three standard olfactory tests: (1) the buried food pellet (BFP) test; (2) the odor choice (OC) test; and (3) the odor cued taste avoidance (OCTA) test.

Apolipoprotein E4 inhibits, and apolipoprotein E3 promotes neurite outgrowth in cultured adult mouse cortical neurons through the low-density lipoprotein receptor-related protein.

The apolipoprotein E4 (apoE4) genotype is a major risk factor for Alzheimer's disease (AD); however, the mechanism is unknown. We previously demonstrated that apoE isoforms differentially modulated neurite outgrowth in embryonic neurons and in neuronal cell lines. ApoE3 increased neurite outgrowth whereas apoE4 decreased outgrowth, suggesting that apoE4 may directly affect neurons in the brain.