Period Concatenation in The Brain, And The Synthesis of Beta 1 Rhythm

The principles of generation of EEG waves in the brain are still ill understood. Although the general mechanism of cortical dipoles and thalamocortical oscillations behind the generation holds true; there has been speculations that the alpha waves could actually be originating in the heart- the cardiac electromechanical hypothesis, which states that the arterial pulse ‘shocks’ the skull-brain mass (and interacts electrically and mechanically) to oscillate at its naturally resonant frequency of approximately 10 Hz.

Now, Kramer et al propose that beta 1 rhythm could be the result of a process called period concatenation (concatenation means chain forming or serial addition). Beta rhythms (18-30 Hz) were thought to be harmonics (integer multiples of the fundamental frequency) of alpha rhythms (8-12 Hz). Kramer et al observed that application of 400 nanomolar kainate to rat somatosensory cortex produced gamma rhythm in the superficial cortical layers and beta2 rhythms in the deep cortical layers.

They observed that after an initial interval of simultaneous gamma (~25 ms period) and beta2 (~40 ms period) rhythms in the superficial and deep cortical layers respectively, a resultant, synchronous beta1 (~65 ms period) rhythm in all cortical layers occurred. They concluded that the time period (the inverse of frequency, or 1/f) of gamma wave (25ms) concatenated with that of beta2 (40ms), to form the time period of 65 ms (40+25). That was the time period of the beta1 rhythm, which resulted as a consequence of this concatenation. They concluded that neural activity in the superficial and deep cortical layers of the brain could combine over time to generate a slower oscillation.

Frequency synthesis would, naturally, have both energy and space saving implications for the system concerned. That the brain economizes is not new in computational biology and electronics. For example, in the simplest and realistic model of the 40 Hz gamma rhythm, only 2 neurons (one excitatory and the other inhibitory) interconnected by reciprocal paths are required. The excitatory neuron will ‘charge’ the inhibitory neuron. The inhibitory neuron will suppress (inhibit) the activity of the excitatory neuron as a result, and any oscillation will be dampened. Hence, a decay in the inhibitory synapse will not inhibit the excitatory neuron anymore and thus cause oscillation; and clearly, the frequency of rhythm will depend on the decay time. This “gamma-motif” resembles a lot with the ‘flip-flop’ circuits in digital electronics.

Its not surprising that the human brain which had evolved as a result of nature’s selection process will learn to compute things so that the metabolic costs of additional neural pacemakers were curtailed to the bare minimum.

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References: Mark A. Kramer, Anita K. Roopun, Lucy M. Carracedo, Roger D. Traub, Miles A. Whittington, Nancy J. Kopell (2008). Rhythm Generation through Period Concatenation in Rat Somatosensory Cortex PLoS Computational Biology, 4 (9) DOI: 10.1371/journal.pcbi.1000169

A Cardiac Hypothesis for the Origin of EEG Alpha
Castillo, Horace T.
Digital Object Identifier: 10.1109/TBME.1983.325080