The Effect of Lanthanum as a Calcium Inhibitor on the CaSR-NSCC Pathway in the Crayfish Neuromuscular Junction

Abstract

Ca²⁺ is a key second messenger in many organisms; this include being essential for neurotransmitter release. Control of extracellular Ca²⁺ ([Ca²⁺]_o) is critical in the human body; imbalances are associated with a large variety of neurological disorders. The Calcium Sensing Receptor (CaSR), the primary mediator in the Ca2+ sensor-nonselective cation channel signaling pathway, detects changes in [Ca²⁺]sub>o, activating a Non-Selective Cation Channel (NSCC) to compensate neurotransmitter release as a response to changes in [Ca²⁺]sub>o. Lanthanides have been found to inhibit NSCC in Arabidopsis thaliana. This study examines the effects of lanthanum on the NSCC in the crayfish neuromuscular junction. We found that the addition of lanthanum increased EPSP amplitudes and durations, thus failing to inhibit the NSCC. This contradicts the results seen in the Arabidopsis thaliana model, which may mean that lanthanides are unable to act as universal NSCC inhibitors or that the CaSR-NSCC signaling pathway operates differently in plants and invertebrate animals.