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J Neurophysiol 77: 186-199, 1997;
0022-3077/97 $5.00
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The Journal of Neurophysiology Vol. 77 No. 1 January 1997, pp. 186-199
Copyright ©1997 The American Physiological Society

Ca2+ Currents in Central Insect Neurons: Electrophysiological and Pharmacological Properties

Dieter Wicher and Heinz Penzlin

Sächsische Akademie der Wissenschaften zu Leipzig, Forschungsgruppe Neurohormonale Wirkungsmechanismen,D-07743 Jena, Germany

Wicher, Dieter, and Heinz Penzlin. Ca2+ currents in central insect neurons: electrophysiological and pharmacological properties. J. Neurophysiol. 77: 186-199, 1997. Ca2+ currents in dorsal unpaired median (DUM) neurons isolated from the fifth abdominal ganglion of the cockroach Periplaneta americana were investigated with the whole cell patch-clamp technique. On the basis of kinetic and pharmacological properties, two different Ca2+ currents were separated in these cells: mid/low-voltage-activated (M-LVA) currents and high-voltage-activated (HVA) currents. M-LVA currents had an activation threshold of -50 mV and reached maximal peak values at -10 mV. They were sensitive to depolarized holding potentials and decayed very rapidly. The decay was largely Ca2+ dependent. M-LVA currents were effectively blocked by Cd2+ median inhibiting concentration (IC50 = 9 µM), but they also had a remarkable sensitivity to Ni2+ (IC50 = 19 µM). M-LVA currents were insensitive to vertebrate LVA channel blockers like flunarizine and amiloride. The currents were, however, potently blocked by omega -conotoxin MVIIC (1 µM) and omega -agatoxin IVA (50 nM). The blocking effects of omega -toxins developed fast (time constant tau  = 15 s) and were fully reversible after wash. HVA currents activated positive to -30 mV and showed maximal peak currents at +10 mV. They were resistant to depolarized holding potentials up to -50 mV and decayed in a less pronounced manner than M-LVA currents. HVA currents were potently blocked by Cd2+ (IC50 = 5 µM) but less affected by Ni2+ (IC50 = 40 µM). These currents were reduced by phenylalkylamines like verapamil (10 µM) and benzothiazepines like diltiazem (10 µM), but they were insensitive to dihydropyridines like nifedipine (10 µM) and BAY K 8644 (10 µM). Furthermore, HVA currents were sensitive to omega -conotoxin GVIA (1 µM). The toxin-induced reduction of currents appeared slowly (tau  ~ 120 s) and the recovery after wash was incomplete in most cases. The dihydropyridine insensitivity of the phenylalkylamine-sensitive HVA currents is a property the cockroach DUM cells share with other invertebrate neurons. Compared with Ca2+ currents in vertebrates, the DUM neuron currents differ considerably from the presently known types. Although there are some similarities concerning kinetics, the pharmacological profile of the cockroach Ca2+ currents especially is very different from profiles already described for vertebrate currents.




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