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The modulation of synaptic strength by long-term depression (LTD) is supposed to be caused by a reduction of presynaptic Ca(2+) currents via mechanisms involving Ca(2+) channel inactivation. We used a combined electrophysiological and computational model of neurones to show that Ca(2+) channel inactivation leads to depression in excitatory (and suppressive) presynaptic transmission also in the case of overstimulation of the axons. The model also showed that similar mechanisms apply to neurones with different Ca(2+) channel subunits. Our results, based on model calculations, are compatible with experimental results on the molecular mechanisms of Ca(2+)-dependent LTD. It is important to note, however, that the model description of Ca(2+) channels is fairly simplistic. The involvement of additional mechanisms in the course of LTD cannot be excluded, but the results from the model show that Ca(2+) channel inactivation is a sufficient mechanism for Ca(2+)-dependent depression in neurones.Financial regulations are hardly ever going to achieve their goals. And in particular, they won’t be able to prevent a crisis from happening, instead they will only be making it harder to deal with it.
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