CHARACTERIZATION OF VOLTAGE-DEPENDENT CALCIUM CURRENTS IN MOUSE MOTONEURONS

1. Calcium channel currents were measured with the whole-cell patch clamp technique in cultured, indentified mouse motoneurons. Three components of current were operationally defined on the basis of voltage dependence, kinetics, and pharmacology. 2. Test potentials to -50 mV or greater (10 mM external Ca2+) elicited a low-voltage activated T-type current that was transient (decaying to baseline in < 200 ms) and had a relatively slow time to peak (20-50 ms). A 1-s prepulse to -45 mV produced approximately half-maximal inactivation of this T current. 3. Two high-voltage activated (HVA) components of current (1 transient and 1 sustained) were activated by test potentials to -20 mV or greater (10 mM external Ca2+). A 1-s prepulse to -35 mV produced approximately half-maximal inactivation of the transient component without affecting the sustained component. 4. When Ba2+ was substituted for Ca2+ as the charge carrier, activation of the HVA components was shifted in the hyperpolarizing direction, and the relative amplitude of the transient HVA component was reduced. 5. Amiloride (1-2 mM) caused a reversible, partial block of the T current without affecting the HVA components. 6. The dihydropyridine agonist isopropyl 4-(2,1,3-benzoxadiazol-4-yl)-1,4-dihydro-2,6-dimethyl-5-nitro-3-pyridinecarboxylate](+)-SDZ 202-791 100 nM-1-mu-M)] shifted the activation of the sustained component of HVA current to more negative potentials and increased its maximal amplitude. Additionally, (+)-SDZ 202-791 caused the appearance of a slowed component of tail current. 7. omega-Conotoxin GVIA (10-mu-M) inhibited the T-type current reverisbly and the two HVA components of calcium current in a partially reversible manner. 8. The presence of omega-conotoxin (10-mu-M) inhibited the (+)-SDZ 202-791-enhanced tail current in some cells (3 of 16) but not in others (13 of 16). These results suggest that some cells express calcium channels that are sensitive to both dihydropyridines and omega-conotoxin.