Regulation of alpha-bungarotoxin receptor accumulation in chick retina cultures: effects of membrane depolarization, cyclic nucleotide derivatives, and Ca2+.

The regulation of a putative neuronal nicotinic acetylcholine receptor, the alpha-bungarotoxin (alpha-Btx)-binding protein, was investigated in primary cultures of chick embryo retina. Depolarization of the cells by veratrum alkaloids, or by a high K+ concentration of the culture medium, reduced the accumulation of cell surface alpha-Btx receptors in these cultures. In contrast, the addition of a blocker of voltage-dependent Na+ channels, tetrodotoxin, increased alpha-Btx receptor accumulation in differentiated retina cultures. Derivatives of cyclic adenosine 3':5'-monophosphate also increased the number of alpha-Btx receptor sites, whereas dibutyryl cyclic guanosine 3':5'-monophosphate, but not 8-bromo-cyclic guanosine 3':5'-monophosphate, had the opposite effect. The blocker of voltage-dependent Ca2+ channels, D600, and media containing a reduced Ca2+ concentration also increased alpha-Btx receptor levels. All of these different culture conditions altered the rate of receptor loss after blocking protein synthesis by cycloheximide. These results show that the synthesis of the neuronal alpha-Btx receptor is regulated by membrane depolarization, cyclic nucleotides, and Ca2+ in a fashion analogous to the regulation of muscle acetylcholine receptor.