Proliferation and differentiation are not directly related to H1(0) accumulation in cultured glial cells.

A basic nuclear chromatin protein with electrophoretic mobility of H1(0) histone is present in C6 rat glial cells and in primary cultures of rat brain astroglial cells. That this protein is identical to H1(0) is further demonstrated by the finding that it accumulates in C6 cells in a time- and dose-dependent manner in response to butyrate, an agent which is known to induce this protein in other cell types. Other short-chain fatty acids were found to influence H1(0) levels similarly although to a lesser extent than butyrate. There was a very close correlation between the induction of H1(0) and the inhibition of growth induced by different concentrations of short-chain fatty acids which supports the idea that the concentration of this protein is higher in non-proliferating cells. However, when cell growth was inhibited by dexamethasone or agents that increase intracellular cyclic adenosine monophosphate levels, H1(0) levels were not affected, even though these compounds also blocked DNA synthesis and induced morphologic changes in C6 cells. These observations suggest that, at least in glial cells, the accumulation of H1(0) is specifically caused by short-chain fatty acids and that suppression of cell division or commitment to differentiation are not sufficient 'per se' for the induction of this protein.