Calcitonin induces a decreased Na⁺ conductance in identified neurons of Aplysia

Abstract

The ionic mechanism of the effect of extracellularly ejected calcitonin (CT) on the membrane of identified neurons R9 and R10 of Aplysia was investigated with voltage-clamp, micropressure ejection, and ion substitution techniques. Micropressure-ejected CT caused a marked hyperpolarization in the unclamped neuron. Heat-inactivated CT was without effect. Clamping the same neuron at its resting potential level (-60 mV) and re-ejecting CT with the same dose produced a slow outward current (Io(CT), 30-40 sec in duration, 4-6 nA in amplitude) associated with a decrease in input membrane conductance. Io(CT) was decreased by depolarization and increased by hyperpolarization. The extrapolated reversal potential of Io(CT) was approximately +10 mV. Io(CT) was sensitive to changes in the external Na+ concentration but not to changes in K+, Ca2+, and Cl- concentrations. Micropressure-ejected forskolin produced a slow outward current, which, like the current to CT, was associated with a decrease in input membrane conductance, and was sensitive to changes in the external Na+ concentration. Io(CT) was prolonged by bath-applied isobutylmethylxanthine (IBMX) but was not affected by 1-oleoyl-2-acetylglycerol (OAG) and calphostin C. Neither superfusion of the neuron with nordihydroguaiaretic acid (NDGA) nor superfusion with indomethacin caused any changes in Io(CT). These results suggest that extracellular CT can induce a slow outward current associated with a decrease in Na+ conductance, mediated by a receptor-controlled increase in intracellular cyclic adenosine 3',5'-monophosphate.

Hormonal Control of Ca Homeostasis in Lower Vertebrates: Considering the Evolution

“…Calcitonin-immunoreactive cells are also found in the abdominal ganglion of sea-hares (Aplysia kurodai). As salmon calcitonin ejected by a micropressure-apparatus caused marked hyperpolarization specifically in some ganglion cells, the calcitonin-like substance may function as a neuromodulator in this ganglion (Sawada et al, 1993).…”

Analgesic effects of calcitonin on radicular pain in male rats

“…The analgesic effects of calcitonin have been confirmed in diseases other than osteoporosis; however, these analgesic effects may be mediated by a different mechanism from that underlying its action as an inhibitor of bone resorption. Calcitonin induces a slow outward current associated with a decrease in sodium conductance causing membrane hyperpolarization in identified neurons of aply-sia 16. We expected calcitonin might have some effects on voltage-dependent sodium channels in the DRG.…”