Induction and expression of long- and short-term neurosecretory potentiation in a neural cell line

Morimoto, Bruce H.; Koshland, Daniel E.

doi:10.1016/0896-6273(90)90347-i

Cited by 136 publications

(98 citation statements)

References 29 publications

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“…To test if the above observation is cell type-specific, we further investigated HT22 cells, a murine central nervous system (CNS) neuronal line (25,26). In contrast to the non-CNS neuroblastoma N2a cells, HT22 cells are derived from mouse hippocampus and therefore better represent brain neurons.…”

Section: Resultsmentioning

confidence: 99%

Single-cell mechanics provides a sensitive and quantitative means for probing amyloid-β peptide and neuronal cell interactions

Lulevich

Zimmer

Hong

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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By using a highly sensitive technique of atomic force microscopybased single-cell compression, the rigidity of cultured N2a and HT22 neuronal cells was measured as a function of amyloid-β42 (Aβ42) protein treatment. Aβ42 oligomers led to significant cellular stiffening; for example, 90-360% higher force was required to reach 80% deformation for N2a cells. Disaggregated or fibrillar forms of Aβ42 showed much less change. These observations were explained by a combination of two factors: (i) incorporation of oligomer into cellular membrane, which resulted in an increase in the Young's modulus of the membrane from 0.9 ± 0.4 to 1.85 ± 0.75 MPa for N2a cells and from 1.73 ± 0.90 to 5.5 ± 1.4 MPa for HT22 cells, and (ii) an increase in intracellular osmotic pressure (e.g., from 7 to 40 Pa for N2a cells) through unregulated ion influx. These findings and measurements provide a deeper, more characteristic, and quantitative insight into interactions between cells and Aβ42 oligomers, which have been considered the prime suspect for initiating neuronal dysfunction in Alzheimer's disease. atomic force microscopy | Alzheimer's disease | cell mechanics | neuronal dysfunction | Young's moduli

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Section: Resultsmentioning

confidence: 99%

Single-cell mechanics provides a sensitive and quantitative means for probing amyloid-β peptide and neuronal cell interactions

Lulevich

Zimmer

Hong

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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“…To test the hypothesis that GR activation by rifampicin accounts for its psychotropic effects, we initially used the mouse cell line HT22 to characterize the interaction of rifampicin with GR. This cell line is derived from the hippocampus (Morimoto and Koshland, 1990), a brain area richly endowed with corticosteroid receptors. Thus, the hippocampus most likely would be a primary target of a GC-like activity of rifampicin.…”

Section: Resultsmentioning

confidence: 99%

“…Mouse clonal hippocampal HT22 cells [a subclone of the HT4 hippocampal cell line (Morimoto and Koshland, 1990)] and human neuroblastoma SK-N-MC cells (American Type Culture Collection no. HTB-10) were kindly provided by the laboratory of C. Behl (Max Planck Institute of Psychiatry, Munich, Germany).…”

Section: Methodsmentioning

confidence: 99%

Rifampicin Is Not an Activator of Glucocorticoid Receptor

et al. 2000

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“…Cell Culture and Treatments-All experiments were performed with rat primary cortical neurons prepared from embryonic day 17 SpragueDawley rats as described previously (21) and with HT22 cells (22), mouse hippocampal cells derived from the HT4 cell line (23). Briefly, primary cortical neurons were dissociated from the cortex and maintained in tissue culture dishes coated with 100 g/ml poly-D-lysine in minimum Eagle's medium supplemented with 30 mM glucose, 2 mM glutamine, 1 mM pyruvate, and 10% fetal bovine serum.…”

Section: Methodsmentioning

confidence: 99%

Fibroblast Growth Factor 1 Regulates Signaling via the Glycogen Synthase Kinase-3β Pathway

Hashimoto

Sagara

Langford

et al. 2002

Journal of Biological Chemistry

119

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We hypothesize that in neurodegenerative disorders such as Alzheimer's disease and human immunodeficiency virus encephalitis the neuroprotective activity of fibroblast growth factor 1 (FGF1) against several neurotoxic agents might involve regulation of glycogen synthase kinase-3␤ (GSK3␤), a pathway important in determining cell fate. In primary rat neuronal and HT22 cells, FGF1 promoted a time-dependent inactivation of GSK3␤ by phosphorylation at serine 9. Blocking FGF1 receptors with heparinase reduced this effect. The effects of FGF1 on GSK3␤ were dependent on phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt) because inhibitors of this pathway or infection with dominant negative Akt adenovirus blocked inactivation. Furthermore, treatment of neuronal cells with FGF1 resulted in ERK-independent Akt phosphorylation and ␤-catenin translocation into the nucleus. On the other hand, infection with wild-type GSK3␤ recombinant adenovirus-associated virus increased activity of GSK3␤ and cell death, both of which were reduced by FGF1 treatment. Moreover, FGF1 protection against glutamate toxicity was dependent on GSK3␤ inactivation by the PI3K-Akt but was independent of ERK. Taken together these results suggest that neuroprotective effects of FGF1 might involve inactivation of GSK3␤ by a pathway involving activation of the PI3K-Akt cascades.Neurotrophic factors are capable of maintaining particular neuronal populations during cellular stress. While some factors, such as nerve growth factor, support a narrowly defined neuronal population (e.g. cholinergic neurons), other factors such as fibroblast growth factor (FGF) 1 support more diverse populations (1). Among the more than 20 members of the FGF family (2, 3), FGF1 (or acidic FGF) is abundant in sensory and motor neurons, and FGF2 (or basic FGF) is primarily produced by astrocytes, although it can be taken up by neurons and translocated to the nucleus (4). Of the four FGF receptors (FGFRs), three are found in the brain: FGFR1 is mainly expressed on neurons, while FGFR2 and FGFR3 are found on glial cells (1, 2, 6, 7). Binding of FGF leads to dimerization of FGFR followed by tyrosine kinase activation (2). FGF2 promotes survival of cortical and hippocampal neurons (8, 9) and is also capable of rescuing neurons from denervation and injury (1). Similarly, FGF1 protects selective neuronal populations against the neurotoxic effects of molecules involved in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (10, 11) and HIV encephalitis (12).FGF1 and -2 are potent regulators of central nervous system development (13, 14) and maintenance after neuronal injury (1). However, there is no consensus as to the signal transduction pathways initiated by FGF during neuronal differentiation or during neuroprotection. Some studies suggest that during FGF2-induced neuronal differentiation (i) activation of a mitogen-activated protein kinase, such as extracellular signal-regulated kinases (ERK1 and ERK2), is neither necessary nor sufficient, (ii) activatio...

show abstract

Induction and expression of long- and short-term neurosecretory potentiation in a neural cell line

Cited by 136 publications

References 29 publications

Single-cell mechanics provides a sensitive and quantitative means for probing amyloid-β peptide and neuronal cell interactions

Single-cell mechanics provides a sensitive and quantitative means for probing amyloid-β peptide and neuronal cell interactions

Rifampicin Is Not an Activator of Glucocorticoid Receptor

Fibroblast Growth Factor 1 Regulates Signaling via the Glycogen Synthase Kinase-3β Pathway

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