http://mscl.cit.nih.gov/homepages/spaj/papers/reprints/generic/dtivd2001.pdf

Water diffusion changes in Wallerian degeneration and their dependence on white matter architecture.

Nerve growth factor (NGF) enhances expression of the cholinergic phenotype observed as increased choline acetyltransferase (ChAT) activity, immunoreactivity, and mRNA. In the present study, treatment of cultured rat embryonic basal forebrain neurons with anti-c-fos, prior to administering NGF, blocked NGF-mediated increases in ChAT activity by 67%; basal ChAT activity was not affected by the antisense oligonucleotide treatment. Reverse transcription-polymerase chain reaction (RT-PCR) revealed that anti-c-fos treatment resulted in not only blockade but enhancement of steady-state ChAT mRNA at different time points. These data suggest that c-fos is an important component in NGF-mediated changes in the cholinergic phenotype and support the hypothesis that c-fos plays a role in the regulation of transcription of the ChAT gene. Elucidation of mechanisms underlying this regulation may aid drug development in neurodegenerative disease.

Molecular mechanisms regulating NGF-mediated enhancement of cholinergic neuronal phenotype: c-fos trans-activation of the choline acetyltransferase gene.

Neurotoxicity of Aβ amyloid protein in vitro is not altered by calcium channel blockade

The ability of the CD44 adhesion molecule to interact with its ligand hyaluronic acid (HA) is tightly regulated. CD44-positive mouse LB lymphoma cells are unable to bind HA unless activated by the tumor promoter phorbol 12-myristate 13-acetate (PMA). PMA causes a dose-dependent increase in both CD44 expression level and HA-binding capacity, with the binding of HA observed only above a threshold amount of CD44 molecules. This induction of HA-binding as well as the increase in CD44 expression are prevented by cycloheximide, suggesting a requirement for new additional CD44 molecules on the cell surface and/or cooperating proteins. In the present study, we have investigated which of the signal transduction pathways activated by PMA leads to the increased CD44 expression with subsequent acquisition of HA-binding capacity. By comparing the influence of each inhibitory agent on PMA-activated LB lymphoma cells versus that on a constitutive HA-binder cell line derived from LB cells (designated HA9 cells), we could distinguish between an effect on the PMA-activation phase and a one on the HA-binding phase. Our data show that the PMA-induced HA-binding could not be blocked by agents inhibiting protein kinase C (PKC) (staurosporine, sphingosine, polymyxin B, quercetin) or genestein, an inhibitor of tyrosine protein kinases. However, this PMA response was strongly inhibited by calmodulin antagonists (chlorpromazine, trifluoperazine, W-7) and the calcium blocker verapamil. The calmodulin antagonists inhibited the PMA-induced increase in CD44 expression on LB cells, but had no influence on the ability of the constitutive HA-binder HA9 cell line to interact with HA, indicating an effect on the PMA induction phase rather than on the binding itself. Verapamil also blocked the PMA-induced increase in CD44 expression on LB cells, but in addition it slightly reduced the ability of the HA9 cells to bind HA without affecting their CD44 expression level. In conclusion, our data suggest that CD44 activation by PMA is calcium and calmodulin dependent, rather than mediated by protein kinase C.

Calcium- and Calmodulin-Dependent PMA-Activation of the CD44 Adhesion Molecule

α-Glycerylphosphorylethanolamine rescues astrocytes from mitochondrial impairment and oxidative stress induced by amyloid β-peptides

Dissociated rat septal nucleus cells cultured in defined medium exhibited twofold increases in the maximal rates of sodium-dependent, high-affinity choline uptake and acetylcholine formation when grown in the presence of phosphoethanolamine. The effect was concentration-dependent (EC50 = 15 microM) and appeared to be associated with in vitro maturation of cholinergic neurons rather than with enhanced survival. Choline acetyltransferase, acetylcholinesterase, and choline kinase activities were unaffected by this treatment. The effect of phosphoethanolamine was specific for cholinergic neurons, because treatment with this compound did not alter the kinetic constants for high-affinity neuronal uptake of gamma-aminobutyric acid or dopamine. The action appeared to be mediated primarily through activation of the sodium-dependent, high-affinity transport mechanism for choline as opposed to alterations in the storage and release of acetylcholine.

Phosphoethanolamine enhances high-affinity choline uptake and acetylcholine synthesis in dissociated cell cultures of the rat septal nucleus.

The synthesis and release of 3H-acetylcholine was measured in hippocampal slices of adult rat brain following acute in vitro exposure to ethanolamine. Evoked release of 3H-acetylcholine was elevated by 60-70% but 3H-acetylcholine synthesis was unaffected. Other amino alcohols were also found to significantly increase evoked 3H-acetylcholine release. The effect may be stereochemically mediated since only one of four possible propanolamine configurations, R-alaninol, was active. The most potent compound tested was R-prolinol which showed an EC50 nearly 10-fold lower than that of either R-alaninol or ethanolamine; S-prolinol was inactive. Slices taken from adult rats which had been fed active compounds for two weeks also exhibited enhancements in evoked 3H-acetylcholine release. These results indicate that amino alcohols modulate acetylcholine release in the rat hippocampus.

Amino alcohol modulation of hippocampal acetylcholine release.

Modulation of acetylcholine release in rat hippocampus by amino alcohols and Bay K 8644.

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Phosphoethanolamine enhances high-affinity choline uptake and acetylcholine synthesis in dissociated cell cultures of the rat septal nucleus.

Amino alcohol modulation of hippocampal acetylcholine release.

Modulation of acetylcholine release in rat hippocampus by amino alcohols and Bay K 8644.