One wrong consequence of forgetting that the charge transfer mechanism is entirely different, the charge carriers are large and heavy (and as a consequence: slow) ions instead of electron (cloud), furthermore they are not necessary present in the volume under test and the ’construction’ of biological matter enables the tested medium to produce charge carriers, using ’equivalent circuits’ for neuronal operation. This fallacy entirely falsifies the conclusions from the measurements.
Another wrong consequence of using ’equivalent circuits’ to describe the electrical operation of neurons is believing that the currents in the biological circuit do not change the concentration, and through the concentration, also the potential; see also section 2.2.2. The ’equivalent circuits’, of course, use a constant potential (they follow the abstraction used in the theory of electricity, although the ’ideal batteries’ also may produce their voltage using chemical processes), and unreasonably, some mystic process changes the resistance/conductance of components. This wrong abstraction results in numerous misunderstandings, among others, introducing ideas such as parallel oscillator equivalent of neuron, input resistance, delayed rectifier current, resting current, and time- or voltage-dependent conductance. Furthermore, we cannot interpret, among others, how neuronal electricity works in lack of external potential; how slow currents operate neuron’s infrastructure, how and why action potential is generated. Deriving the time course of the Nernst-Planck potential opens the way to a quantitative understanding of neurophysical electrical processes, including their time course.
Again another wrong consequence is that the two secondary abstractions ’potential’, and ’current’, became independent from the primary abstraction ’charge’ and each other (significantly contributing to the fallacy that ’physics cannot describe life’). Our equations and the underlying discussion point to the fact that the potential and the current cannot be separated from the charge. No ’delayed rectifying current’ and ’voltage- (or time-) dependent conductance’ exist. Those notions originate from the wrong interpretation of measured data derived from mismatching measured electrical data pairs and the misconception that biological structures and materials must behave like metals.
As we discussed in section 2.6.5, the unbalanced charge in neurons and the charge injected suddenly into the intracellular segment during a rush-in action are in the same order of magnitude. We also discussed that the charge injection (the appearance and flow of charge in the proximal layer on the membrane’s surface) causes well measureable mechanical, optical, etc. changes [95] on the membrane. Those changes are well observable on the low-concentration side, in the form of slow currents, and large-scale concentration and potential changes.
Those changes also mean that a large amount of charge passes from the high-concentration side to the low concentration side of the membrane, and causes a sudden drop on the high-concentration side of the membrane. As discussed, that change means simultaneously a change in the corresponding potentials across the membrane that solves the mystery why the AP AP stops. The potential across the membrane is defined by the difference of the potential of the two thin layers (see section 2.8.4) on the membrane’s surface. As we discussed, a huge electric field exists across the plates of the neuronal condenser, while a moderate one in the proximal layers. That means that the ions can quickly leave the high concentration when the rush-in injection begins. They produce an ’empty’ layer (and a potential gradient) whithin that layer and the ions in the neighboring layer start to move using the ’downhill’ potential. However, they do have a much slower speed, so they ’stop’ at some distance.