Brain cells process thoughts (energy) of different class and quality in an area-specific manner. The NaAF-driven Na-pump is the voltage generator across brain cell plasma membrane, hence is the earliest electromagnetic-boundary (or gate) that the area-specific thought signals (electromagnetic) encounter. The human body is essentially a bundle of electromagnetic energy that owes its very existence to the presence of abundant inorganic ions (~ 300 mM) distributed differently between the cells and circulating blood where the semipermeable plasma membranes having Na, K-ATPase pumps act as the differential ion barrier. Function of the dual-channel Na-pump (Na, K-ATPase) fully depends on a ubiquitous cytosolic regulator, NaAF of 170 k Da mass maintaining the ion gradient (or electromagnetic potential) for carrying out numerous interlinked processes. Energy and information continually flows through this intricate intra- and inter-cellular network in order to maintain the mind-body functions supervised by the brain.
NaAF being the first molecular driver of the Na, K-ATPase pump, it is likely to be the natural mediator of transcendental Will-power (electromagnetic thought-signals). Different areas of the brain containing different αβ-isoforms of the Na, K-ATPase have differential affinities towards Na, K, Ca and ATP. Hence, the nature and intensity of the area-specific thought-signals will be handled with different efficacy during transmission of the signal. Following depolarization those Na-pumps at the synaptic junction acting as provisional Ca-pumps (in altered states) to drive out excess Ca (> 10 µM), will also show differential activities towards Ca based on isoform (αβ)-nature, affecting time for repolarization and the signal flow.
Expectedly, the ubiquitous NaAF maintains its own intracellular level via gene-expression (on demand basis) in all cell types. In brain the sublime Will-power (opener of thought signal) may additionally influence the cell NaAF level by microRNAs at the level of translation (from mRNA level). This is based on recent evidences on heart-pump related signaling proteins in cardiac hypertrophy (Rooiz et al PNAS 105, 13027–13032, 2008) and heart failure.