Characteristics of transcriptionally active and inactive neuronal and nonastrocytic glial rat brain chromatin fractions.

Rapid and reliable fractionation of neuronal and nonastrocytic glial (NAG) cerebral rat brain chromatin in transcribable and repressed portions was achieved employing the DNAase II/Mg++-solubility method of Gottesfeld et al. (1974). Compositional and transcriptional properties of these fractions have been investigated.

Repression of glial RNA transcription during the development of 6-aminonic-otinamide (6-AN)-induced acute gliopathy.

Administration of 6-aminonicotinamide (6-AN) to rats leads to an opposite effect on the rate at which [3H]UMP is incorporated in vitro into nuclear cerebral neuronal and glial RNA. The inhibition of glial RNA synthesis is temporarily accompanied by both a reduction of the number of RNA initiation sites on glial chromatin and a reduction of [3H]acetate uptake into glial chromatin-bound histones mainly as regards the fraction H2B, H3 and H4. The slight stimulation of neuronal RNA synthesis 6 hours after 6-AN seemed to be caused exclusively by a less steric restriction of neuronal chromatin, whereas the more pronounced stimulation at 24 hours may be related to both a higher activity and/or amount of endogenous neuronal RNA polymerases and an increase in the total number of RNA initiation sites present on the neuronal chromatin.

Studies on the regulation of RNA synthesis in neuronal and glial nuclei isolated from rat brain.

In searching for regulatory mechanisms involved in the cell-specific neuronal and glial transcription a cell-free transcriptional system has been developed using neuronal and glial rat brain chromatin and partially purified neuronal and glial nuclear rat brain RNA polymerases. Both free and chromatin-bound (engaged) neuronal and glial RNA polymerase fractions were separated from isolated neuronal and glial rat brain nuclei to determine their transcriptive efficiency. A double number of RNA initiation sites was measured on the neuronal when compared to the glial chromatin, independently of whether the neuronal or the glial RNA polymerase preparation was used for the determination.

On the mechanism of lanthanide-induced liver toxicity.

The intravenous injection of the lighter lanthanide ions Pr(III), Nd(III), and Sm(III) in doses of 35 mumoles/kg inhibits, and isoosmolar doses of the heavier lanthanide ions Gd(III), Dy(III), and Er(III) stimulate rat liver nuclear in vitro RNA synthesis catalyzed by RNA polymerase B 24 h after their application, while nuclear RNA synthesis, catalyzed by RNA polymerase A, was inhibited by the same isoosmolar doses of Pr(III), Nd(III) and not influenced by Sm(III), Gd(III), Dy(III), or Er(III). The effect of in vivo applied Pr(III) and Nd(III) on rat liver in vitro nuclear RNA synthesis shows a similar time and dose-dependent pattern. The decreased rat liver nuclear in vitro RNA synthesis 24 h after intravenous injection of Pr(III) as well as after Nd(III) was accompanied by a decreased nuclear in vitro 3H-acetate uptake by the chromatin-bound histone fractions, F 2a2, F 3, and F 2al.