Abstract
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. The increase in the total number of neuronal RNA initiation sites is closely parallel with a higher degree of acetylation of neuronal chromatin-bound histone fractions. The 6-AN-induced variations of glial and neuronal in vitro RNA synthesis are discussed in correlation with the neurotoxic action of 6-AN in vivo.
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Repression of glial RNA transcription during the development of 6-aminonic-otinamide (6-AN)-induced acute gliopathy.
