Nonsynaptic plasticity model of long-term memory engrams.

Using steady-state electrical properties of non-ohmic dendrite based on cable theory, we derive electrotonic potentials that do not change over time and are localized in space. We hypothesize that clusters of such stationary, local and permanent pulses are the electrical signatures of enduring memories which are imprinted through nonsynaptic plasticity, encoded through epigenetic mechanisms, and decoded through electrotonic processing. We further hypothesize how retrieval of an engram is made possible by integration of these permanently imprinted standing pulses in a neural circuit through neurotransmission in the extracellular space as part of conscious recall that acts as a guiding template in the reconsolidation of long-term memories through novelty characterized by uncertainty that arises when new fragments of memories reinstate an engram by way of nonsynaptic plasticity that permits its destabilization. Collectively, these findings seem to reinforce this hypothesis that electrotonic processing in non-ohmic dendrites yield insights into permanent electrical signatures that could reflect upon enduring memories as fragments of long-term memory engrams.

Induced mitochondrial membrane potential for modeling solitonic conduction of electrotonic signals.

A cable model that includes polarization-induced capacitive current is derived for modeling the solitonic conduction of electrotonic potentials in neuronal branchlets with microstructure containing endoplasmic membranes. A solution of the nonlinear cable equation modified for fissured intracellular medium with a source term representing charge 'soakage' is used to show how intracellular capacitive effects of bound electrical charges within mitochondrial membranes can influence electrotonic signals expressed as solitary waves. The elastic collision resulting from a head-on collision of two solitary waves results in localized and non-dispersing electrical solitons created by the nonlinearity of the source term. It has been shown that solitons in neurons with mitochondrial membrane and quasi-electrostatic interactions of charges held by the microstructure (i.e., charge 'soakage') have a slower velocity of propagation compared with solitons in neurons with microstructure, but without endoplasmic membranes. When the equilibrium potential is a small deviation from rest, the nonohmic conductance acts as a leaky channel and the solitons are small compared when the equilibrium potential is large and the outer mitochondrial membrane acts as an amplifier, boosting the amplitude of the endogenously generated solitons. These findings demonstrate a functional role of quasi-electrostatic interactions of bound electrical charges held by microstructure for sustaining solitons with robust self-regulation in their amplitude through changes in the mitochondrial membrane equilibrium potential. The implication of our results indicate that a phenomenological description of ionic current can be successfully modeled with displacement current in Maxwell's equations as a conduction process involving quasi-electrostatic interactions without the inclusion of diffusive current. This is the first study in which solitonic conduction of electrotonic potentials are generated by polarization-induced capacitive current in microstructure and nonohmic mitochondrial membrane current.