Intracellular electrophysiological evidence: how pain is experienced by neurons

Abstract

The aim hereof is to identify changes in the performance of the CNS neurons under the prolonged action of low-threshold pain factor according to indicators of the membrane potential level, parameters of the action potential and the pattern of the firing activity distribution of the neurons.

Aims

The aim hereof is to identify changes in the performance of the CNS neurons under the prolonged action of low-threshold pain factor according to indicators of the membrane potential level, parameters of the action potential and the pattern of the firing activity distribution of the neurons.

Materials and methods

As a model, functionally active neurons of the central nervous system in the grape snail Helix pomatia were selected as an integral part of the organism in vivo. Used has been the author’s original electrophysiological method of continuous recording of intracellular biopotentials of animal neurons both under the background conditions and by applying a long-term low-threshold action (LTA) to the main nerves due to a graded pressure to produce a pain effect of the subthreshold level that over time turns into increasing pain.

Results

For the first time in world science, objective evidence for the long-term low-intensity action of pain on the electrophysiological characteristics in a CNS neuron has been obtained. Revealed are the changes in the amplitude and the action potential firing rate, the membrane potential level and the pattern of the neuron pulse activity, traced continuously, up to full neuron potential turning-off. It has been detected that, when removing the pain factor, there are some points of return to the norm available, and, in case of longevity of the pain action, the functional state of the neuron passes the point of no return, after which the neuron electrophysiological potentials reach zero value, indicating the cessation of its life.

Conclusions

The dynamics of the neuron functional state in vivo, under prolonged action of the pain factor, reflects nonlinear changes in the membrane potential, firing rate and amplitude of AP. This characterizes the phase process of forming a pathologically stable pain state of the neuron, despite the readiness of the membrane mechanisms at the transition points to a response aimed at returning to life. The evidence obtained in our experiments provides more insight into the mechanisms of chronic neurogenic pain in experimental and clinical medicine, as well as the diagnostics of the brain death.

Imprint

Valery I. Orlov, Alla I. Shikhlyarova. Intracellular electrophysiological evidence: how pain is experienced by neurons. Cardiometry; Issue 17; November 2020; p.8-21; DOI: 10.12710/cardiometry.2020.17.821; Available from: http://www.cardiometry.net/issues/no17-november-2020/electrophysiological-evidence