Change in amplitude of slow depolarization of GABA (A) – and glutamate receptor

Abstract

The termination of a bundle of action potentials is performed by increasing [Ca2+]i and activating
Ca2+ -dependent K+ channels, closing potential-dependent Ca2+ -channels and inactivating them. As a
result, the membrane is even more hyperpolarized (10 mV below the critical potential), which leads to
suppression of the generation of action potentials, activation of HCN-like channels and the re-activation
of 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, during
which 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 impulse
of 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. The
suppression of T-type activity of Ca2+ channels decreases the duration of the Ca2+ pulse at spontaneous
synchronous activity of neurons, which can contribute to the survival of neurons during hyper-excitation
and ischemia. Thus, the decrease in the duration of the Ca2+ pulse when T-type inhibitors are activated
by 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.