Harnessing Electroceuticals to Treat Disorders Arising From Traumatic Stress: Theoretical Considerations Using A Psychosensory Model.

Traumatically encoded memories can last a lifetime. These memories, either by purposeful or inadvertent re-activation, cause the release of stress hormones and generate a persistent and inescapable allostatic load on the body, brain and mind. This leads to a maladaptive response, as the ability to return to pre-event homeostasis is no longer possible. The consequence of this response is that it increases risk for further traumatization and other disorders. Remarkably, recent research has shown that these memories become labile and subject to disruption upon recall. In this paper we outline conditions needed for an event to be encoded as a trauma and describe a method that abrogates the release stress hormones when cued by these memories of the event. Critical to this process is the AMPA receptor (so named for its specific agonist, AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, a compound that acts as glutamate, its natural substrate). It is hypothesized that traumatic encoding requires increasing the number and permanence of AMPA receptors on the lateral nucleus of the amygdala by a process called synaptic potentiation. Depotentiation, that is removal of these AMPA receptors, is required for de-encoding. We speculate that the generation of oscillatory intracellular calcium waves is necessary for this to occur. Electromagnetic fields, acting as electroceuticals, interact with voltage-gated calcium channels on depolarized post-synaptic membranes to produce these intracellular calcium oscillations of varying frequency. These oscillatory calcium waves are decoded by intracellular calmodulin which, depending on the frequency, either act to potentiate or depotentiate AMPA receptors. This article describes the theory and practical application of a psychosensory approach called Event Havening that generates an electromagnetic field to synaptically depotentiate these encoded AMPA receptors and eliminate the effects of traumatic encoding.

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