Rhythmicity of Biopotentials: Its Origin and Involvement in Information Processing

Abstract

Experimental data and mathematical simulation of a neural network were used to develop ideas concerning the origin of the rhythmicity of biopotentials and its involvement in information processing. Baseline slow oscillations—the primate α rhythm, the α-like rhythms of lower animals, the Δ rhythm of humans and animals, secondary components of sensory evoked potentials or responses to direct brain stimulation, and pathological epileptiform potentials—develop as a result of interactions between excitatory and inhibitory postsynaptic potentials. The main inhibitory transmitter in the brain cortex is γ-aminobutyric acid (GABA). EEG activation in the form of a decrease in the amplitude of baseline oscillations and the appearance of the stress rhythm in the θ band upon exposure to new or biologically significant stimuli is associated with a relative decay of inhibitory hyperpolarization processes. The cholinergic and noradrenergic neurotransmitter systems are substantially involved in the rearrangement of the neural activity associated with EEG activation. An enhancement of high-amplitude baseline oscillations and phasic activity of neurons, i.e., alternation of activation and inhibition of firing, which reflects a relative enhancement of hyperpolarization processes, restricts excitation propagation over brain structures and impedes the fixation of new information. As a result of the decay of the inhibitory processes, EEG activation is accompanied by a higher regularity of neuronal firing and a decrease in entropy in the time distribution of firing in the form of tonic or grouped (in the stress rhythm) discharges. The resulting ordered streams of impulses transfer information, control its propagation, and ensure its fixation and reproduction.