During the training, the membrane potential becomes more and more polarized with strong negative values on the classes that are not recognized by the selected neuron.
An example of membrane potential dynamics is shown in Figure 2. When P t >P threshold, the neuron fires a spike, the membrane potential becomes P t =P refract (resting potential) and a refractory period counter starts.
NCX easily reverses its direction and brings Ca2+ into the cells if the Na+ concentration gradient decreases and/or the membrane potential becomes less negative.
As shown in Figure 5A1, the membrane potential became more hyperpolarized when Na+ was substituted with equimolar NMDG+ in all the control groups, but no significant change was observed in the U-type dsRNA or siRNA groups.
When the membrane potential became stable, at a value lying between –40 and –60 mV, the negative pressure was released, in order to avoid sucking in the intracellular contents.
By 6 8 days, myocytes began to divide while completely losing their distinctive cardiac electrical phenotype: the inward rectifier potassium current (IK1) virtually disappeared, resting membrane potential became depolarized, and cells shrank as revealed by decreased electrical capacitance (Figure 2).
As learning progressed and higher and lower affinity receptors were eliminated (Fig. 3B), the neuron's membrane potential became more sensitive to glutamate concentration (Fig. 3B, compare last cycle in black to first cycle in red).
Addition of IAA to the incubation medium (Table 1, Fig. 6) caused transient depolarization of the Em, followed by a delayed hyperpolarization, during which membrane potential became more negative than the original potential.
In other terms, the stochastic components of the membrane potentials become perfectly synchronized, therefore from now on we refer to this phenomenon as stochastic synchronization.
It is shown theoretically that the membrane potential enhancement becomes greater with decreasing the electrolyte concentration and pore radius.
In response to the loss of mitochondrial membrane potential, PINK1 becomes stabilized at the outer mitochondrial membrane where it can interact and phosphorylate parkin for its recruitments and activation at the site of mitochondria (Kane et al., 2014; Kazlauskaite et al., 2014; Koyano et al., 2014; Lazarou et al., 2015; Matsuda et al., 2010; Pickrell and Youle, 2015).
