The action potential: an effect of fuel cell reactions in the synapse.

The neuron and its vascular-interstitial communications form, in vivo, an electrophoretic closed circuit. It is charged by ionic pumps in the nerve cell membrane at rest. Electrophoretic products of reaction collect at biologic electrodes, represented by redox proteins. These are located in the pre- and postsynaptic membranes and also in associated capillary membranes in the vascular part of the closed circuit. Efferent brain impulses start a series of events preceding muscle contraction. They open ionic channels in the membrane of the nerve cell body. A short-circuiting is thereby created, and cations flow into the cell. The membrane pumps cannot withstand this ionic inflow and maintain the transmembranous potential difference. The circuit is no longer driven but starts selfdriving reactions by previously formed products of reaction at the biological electrodes. Fuel cell reactions start at these and create in the axon the peak of the action potential. In vivo, the action potentials preceding the contracting of a muscle are transmitted through the circuit. In the vascular pathway of the closed circuit, the action potentials appear, by summation, as the previously described slow potential waves. The function of nerve cell matrices, as well as the nodes of Ranvier, are discussed. The proposed theory is in accordance with the vascular-interstitial-neuromuscular closed circuit. It provides new possibilities to explain the development of the action potential, transport and disappearance of various synaptic structures and the neurotransmitter. Technical analogues are presented to illustrate a new possible background mechanism for understanding structure and function in neuromuscular transmission.