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  • 1
    Keywords: RECEPTOR ; EXPRESSION ; IN-VITRO ; PROTECTION ; Germany ; IN-VIVO ; VITRO ; VIVO ; SYSTEM ; SYSTEMS ; NEW-YORK ; MICE ; MECHANISM ; mechanisms ; TYPE-1 ; ACID ; NERVOUS-SYSTEM ; DAMAGE ; CENTRAL-NERVOUS-SYSTEM ; MUTANT MICE ; max ; ACUTE NEURONAL INJURY ; ANANDAMIDE ; ENDOCANNABINOIDS ; GLUTAMATE ; N-ACYLETHANOLAMINE PHOSPHOLIPIDS ; NEUROPROTECTION ; RAT-BRAIN ; SEIZURE
    Abstract: Abnormally high spiking activity can damage neurons. Signaling systems to protect neurons from the consequences of abnormal discharge activity have been postulated. We generated conditional mutant mice that lack expression of the cannabinoid receptor type 1 in principal forebrain neurons but not in adjacent inhibitory interneurons. In mutant mice, the excitotoxin kainic acid (KA) induced excessive seizures in vivo. The threshold to KA-induced neuronal excitation in vitro was severely reduced in hippocampal pyramidal neurons of mutants. KA administration rapidly raised hippocampal levels of anandamide and induced protective mechanisms in wild-type principal hippocampal neurons. These protective mechanisms could not be triggered in mutant mice. The endogenous cannabinoid system thus provides on-demand protection against acute excitotoxicity in central nervous system neurons
    Type of Publication: Journal article published
    PubMed ID: 14526074
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  • 2
    Keywords: ACTIVATED PROTEIN-KINASE ; PROGRAMMED CELL-DEATH ; ISOLATED RAT HEPATOCYTES ; ENDOPLASMIC-RETICULUM STRESS ; CHAPERONE-MEDIATED AUTOPHAGY ; BREAST-CANCER CELLS ; STARVATION-INDUCED AUTOPHAGY ; VACUOLE TARGETING PATHWAY ; GLUCAGON-INDUCED AUTOPHAGY ; BETAINE HOMOCYSTEINE METHYLTRANSFERASE
    Abstract: In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.
    Type of Publication: Journal article published
    PubMed ID: 22966490
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  • 3
    ISSN: 1435-1463
    Keywords: Keywords:α-Tocopherol, vitamin E, 17-β estradiol, oxidative stress, glutamate, NF-κB, neuroprotection.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. Antioxidants can function as powerful protectants for neurons in vitro. Here, the neuroprotective activity of lipophilic free radical scav-engers synthetic (±) α-tocopherol (synthetic vitamin E) and natural (+) α-tocopherol (natural vitamin E) against oxidative stress was investigated and compared to the neuroprotective effect of the female sex hormone estradiol. Employing mouse clonal hippocampal HT22 cells and rat cerebellar granule neurons, we found that both types of α-tocopherol exerted a higher neuroprotective antioxidant activity than 17-β estradiol. At concentrations as low as 100 nM, synthetic (±) α-tocopherol and natural (+) α-tocopherol protected neurons effectively against the oxidative cell death caused by the Alzheimer's disease-associated amyloid β protein, hydrogen peroxide, and the excitatory amino acid glutamate. Moreover, vitamin E induced the activity of the redox-sensitive transcription factor NF-κB, which is involved in the control of nerve cell survival and, therefore, may play also a role in vitamin E-induced neuroprotection. These results may have implications regarding the prevention and treatment of oxidative stress-related degenerative disorders such as Alzheimer's disease.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Cell & tissue research 290 (1997), S. 471-480 
    ISSN: 1432-0878
    Keywords: Key words: Amyloid β-protein ; Neurotoxicity ; Alzheimer’s disease ; Oxidative stress ; Antioxidants ; Neuroprotection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by loss of memory and progressive decline of cognitive abilities. Although the pathogenesis of this disease is not known and is still under intensive investigation, there are several hypotheses which address certain aspects of the disease. This review focuses on the oxidative-stress hypothesis of AD and on novel antioxidative approaches to an effective neuroprotection for the prevention and therapy of this neurodegenerative disorder. The toxicity of the AD-associated amyloid β-protein (Aβ), the induction of oxidative stress by Aβ in neurons, and potential sources of oxidative events in brain tissue are discussed.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Effects of estrogen hormones on lipid peroxidation (LPO)were examined in rat brain homogenates (RBHs), hippocampal HT 22 cells, ratprimary neocortical cultures, and human brain homogenates (HBHs).Dose-response curves indicated half-maximal effective concentrations(EC50) of 5.5 and 5.6 mM for iron-induced LPO in RBHs andHT 22 homogenates. Incubation of living rat primary neocortical cultures withiron resulted in an EC50 of 0.5 mM, whereas culturehomogenates showed an EC50 of 1.2 mM. Estrogen hormonesreduced LPO in all systems: In RBHs, estrone inhibited iron-induced LPO to74.1 ± 5.8% of control levels (17β-estradiol: 71.3 ± 0.1%)at a concentration of 10 μM. In hippocampal HT 22 cellhomogenates, levels of LPO were reduced to 74.8 ± 5.5% by estrone andto 47.8 ± 6.2% by 17β-estradiol. In living neocortical cultures,17β-estradiol decreased iron-induced LPO to 79.2 ± 4.8% andincreased the survival of cultured neuronal cells. Of the other steroidcompounds tested (corticosterone, progesterone, testosterone), onlyprogesterone decreased LPO in HT 22 cell homogenates. In HBHs, LPO wasdose-dependently increased by iron concentrations from 2.7 to 6.0 mM.Incubation with estrogens resulted in a dose-dependent inhibition of LPO to53.89 ± 8.6% with 10 μM 17β-estradiol, whereas estrone failed to affect iron-induced LPO to a significant extent. Nonestrogenic steroids, including hydrocortisol, did not show significant effects on LPO in HBHs.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 107 (2000), S. 1325-1344 
    ISSN: 1435-1463
    Keywords: Keywords: Alzheimer's disease, apoptosis, necrosis, caspase.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. Cell death by apoptosis comprises a sequence of events leading to the activation of caspases. Caspases execute the fragmentation of the cellular protein and DNA, ultimately, leading to disintegration of the cell. Apoptosis is a tightly regulated physiological mechanism that is crucial during development and thereafter for the maintenance of the balance between cell division and cell death. In contrast to the rather smoothly operating cell death machinery of apoptosis, necrosis is caused by insults leading to the rapid disruption of cellular metabolism and the non-physiological disintegration of the cells. Frequently, toxic events or traumatic challenges trigger the rapid necrotic cell death. Apoptosis and necrosis can be discriminated by a number of morphological and biochemical characteristics. To describe the specific mechanisms of cell death occurring during neurodegenerative disorders, such as Alzheimer's disease (AD), many investigations, both in vivo and in vitro, have attempted to label the particular pathway of cell death either as apoptosis or as necrosis. The elucidation of the mechanism of cell death promises to identify novel pharmaceutical targets for the prevention and therapy of AD. Apoptotic and necrotic cells can be found in AD tissue, and both pathways can be mimicked employing a variety of models systems of AD-associated nerve cell degeneration. Certain genes that are linked to familial AD may render neurons more vulnerable to apoptosis, but it has to be stressed that the vast majority of AD cases are sporadic and not strictly genetically determined. Apoptosis and necrosis may overlap, may sequentially occur under certain conditions, and may not be detected unequivocally. In conclusion, on the basis of the presently available data it has to be stated that although many studies in vivo and in vitro favor apoptosis in AD, there is considerable evidence that a mixture of both events may contribute to neurodegeneration in AD and to its final pathology.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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