Abstract
The termination of a bundle of action potentials is performed by increasing [Ca2+]i and activatingCa2+ -dependent K+ channels, closing potential-dependent Ca2+ -channels and inactivating them. As aresult, the membrane is even more hyperpolarized (10 mV below the critical potential), which leads tosuppression of the generation of action potentials, activation of HCN-like channels and the re-activationof Na+ – and potential-dependent Ca2+ -channels. The activity of HCN-like channels is increasing, the membrane is slowly depolarizing and reaches the critical potential of the excitation process, duringwhich the generation of the tonic action potentials begins, and then the Ca2+ -channel begins to re-generate the process and the process begins. Consequently, calcium channels, which determine the impulseof slow depolarization, control the frequency and amplitude of the potentials of action during spontaneous synchronic activity, regulating the conditions of activation and inactivation of Na+ channels. Thesuppression of T-type activity of Ca2+ channels decreases the duration of the Ca2+ pulse at spontaneoussynchronous activity of neurons, which can contribute to the survival of neurons during hyper-excitationand ischemia. Thus, the decrease in the duration of the Ca2+ pulse when T-type inhibitors are activatedby the Ca2+ channel may be one of the well-known neuroprotector effects of these compounds.Key words: calcium pulse, C2+ channels, potential of action, genesis, depolarization.