Decreased calcium concentration increases magnitude and time course of facilitation but decreases time course of depression following long-term high frequency stimuli

Abstract

Calcium is a ubiquitous second messenger in neurotransmitter release pathways, but the specific mechanisms of its regulation of synaptic plasticity are still a topic of debate. Our study further clarifies the effects of low calcium concentration on the magnitude and time course of initial synaptic facilitation and subsequent depression resulting from long-term high frequency stimulation at the crayfish neuromuscular junction. Our results contradict previous studies that suggest increased levels of pre-synaptic calcium concentration result in increased magnitude and time course of facilitation. These contradictory results may implicate additional roles for calcium, not only as a second messenger, but also as a buffer ion used to shield the surface charge of cells, thus maintaining a high neuronal threshold. Our results agree with the vesicle depletion hypothesis, that lower levels of calcium leads to a decreased time course of depression.