EFFECTS OF GANGLIONIC SATELLITE CELLS AND NGF ON THE EXPRESSION OF NICOTINIC ACETYLCHOLINE CURRENTS BY RAT SENSORY NEURONS

1. We have investigated two factors that affect the expression of nicotinic acetylcholine (ACh) currents on neonatal rat sensory neurons: an influence derived from ganglionic satellite cells, and nerve growth factor (NGF). 2. With the use of whole-cell patch-clamp techniques on rat nodose neurons, we have measured the proportion of neurons sensitive to ACh and have quantified their ACh current densities. The majority (60%) of nodose neurons from neonatal animals do not express nicotinic acetylcholine receptors (nAChRs); the remaining 40% had ACh current densities that ranged from 0.4 to 93 pA / pF. Furthermore, neither the proportion nor the ACh current densities change over the first two postnatal weeks in vivo. 3. The expression of ACh currents by these neurons in vivo is controlled, in part, by an influence from the ganglionic satellite cells: culturing neurons in the absence of other cell types results in an increase in the proportion of ACh-sensitive neurons, whereas coculturing neurons with their satellite cells maintains functional nAChR expression in its in vivo state. Furthermore, satellite cells are not required continually, as a brief exposure to this influence, either in vivo or in culture, is sufficient to exert its effect on functional nAChR expression. 4. On removal of this satellite cell influence, the neurons respond to NGF treatment by increasing their ACh current densities: the median ACh current density for neurons grown for 2-3 wk with NGF was 32.5 pA / pF, whereas, the median ACh current density for neurons cultured without NGF for the same time was 4.5 pA / pF. In addition, NGF must be continually present to sustain this increase. 5. Our experiments indicate that the expression of ACh currents by nodose neurons is controlled by their ganglionic satellite cells, and that NGF, operating through a different mechanism, regulates ACh currents densities on ACh-sensitive neurons in the absence of this satellite cell influence.