EXTRINSIC FACTORS INFLUENCE THE EXPRESSION OF VOLTAGE-GATED K-CURRENTS ON NEONATAL RAT SYMPATHETIC NEURONS

Voltage-gated potassium (K) currents are important in controlling a ne uron's excitability. We have shown previously (McFarlane and Cooper, 1 992) that neonatal superior cervical ganglia (SCG) neurons express thr ee voltage-gated K currents: a noninactivating delayed-rectifier type current (I(K)), a rapidly inactivating A-current (I(Af), and a slowly inactivating A-current (I(As)). When grown in culture for 4 weeks with out other cell types, SCG neurons lose their expression of I(A), and I (As), suggesting that an extrinsic factor(s) is involved in controllin g the expression of these currents. In vivo, SCG neurons are surrounde d by non-neuronal cells. Therefore, in this study we investigated whet her the ganglionic non-neuronal cells provide a factor required for A- current expression. We show that postnatal day 1 (P1) SCG neurons cont inue to express I(Af) and I(As) when cocultured with their ganglionic non-neuronal cells. Medium conditioned by ganglionic non-neuronal cell s mimics the non-neuronal cell influence on I(Af) and I(As) expression , suggesting that the effects of non-neuronal cells are mediated by wa y of a secreted factor. Ciliary neurotrophic factor, a factor present in peripheral non-neuronal cells, has similar effects to those of gang lionic cell-conditioned medium. Moreover, we find that the dependence of I(Af) on a non-neuronal cell factor is developmentally regulated; P 14 neurons grown in culture without other cell types continue to expre ss I(Af). However, I(As) on P14 neurons maintains its dependence on a factor from non-neuronal cells. Finally, in addition to extrinsic cont rol of voltage-gated K currents, we suggest that SCG neurons use intri nsic mechanisms to coordinate their expression of I(Af), I(As), and I( K) such that changes in one K current are compensated for by reciproca l changes in one or more of the other K currents.