RETRACTED: Mechanisms Contributing to the Generation of Mayer Waves

Abstract

Mayer waves may synchronize overlapping propriobulbar interneuronal microcircuits constituting the respiratory rhythm and pattern generator, sympathetic oscillators, and cardiac vagal preganglionic neurons. Initially described by Sir Sigmund Mayer in the year 1876 in the arterial pressure waveform of anesthetized rabbits, authors have since extensively observed these oscillations in recordings of hemodynamic variables, including arterial pressure waveform, peripheral resistance, and blood flow. Authors would later reveal the presence of these oscillations in sympathetic neural efferent discharge and brainstem and spinal zones corresponding with sympathetic oscillators. Mayer wave central tendency proves highly consistent within, though the specific frequency band varies extensively across, species. Striking resemblance of the Mayer wave central tendency to the species-specific baroreflex resonant frequency has led the majority of investigators to comfortably presume, and generate computational models premised upon, a baroreflex origin of these oscillations. Empirical interrogation of this conjecture has generated variable results and derivative interpretations. Sinoaortic denervation and effector sympathectomy variably reduces or abolishes spectral power contained within the Mayer wave frequency band. Refractorines of Mayer wave generation to barodeafferentation lends credence to the hypothesis these waves are chiefly generated by brainstem propriobulbar and spinal cord propriospinal interneuronal microcircuit oscillators and likely modulated by the baroreflex. The presence of these waves in unitary discharge of medullary lateral tegmental field and rostral ventrolateral medullary neurons (contemporaneously exhibiting fast sympathetic rhythms [2–6 and 10 Hz bands]) in spectral variability in vagotomized pentobarbital-anesthetized and unanesthetized midcollicular (i.e., intercollicular) decerebrate cats supports genesis of Mayer waves by supraspinal sympathetic microcircuit oscillators. Persistence of these waves following high cervical transection in vagotomized unanesthetized midcollicular decerebrate cats would seem to suggest spinal sympathetic microcircuit oscillators generate these waves. The widespread presence of Mayer waves in brainstem sympathetic-related and non-sympathetic-related cells would seem to betray a general tendency of neurons to oscillate at this frequency. We have thus presented an extensive and, hopefully cohesive, discourse evaluating, and evolving the interpretive consideration of, evidence seeking to illumine our understanding of origins of, and insight into mechanisms contributing to, the genesis of Mayer waves. We have predicated our arguments and conjectures in the substance and matter of empirical data, though we have occasionally waxed philosophical beyond these traditional confines in suggesting interpretations exceeding these limits. We believe our synthesis and interpretation of the relevant literature will fruitfully inspire future studies from the perspective of a more intimate appreciation and conceptualization of network mechanisms generating oscillatory variability in neuronal and neural outputs. Our evaluation of Mayer waves informs a novel set of disciplines we term quantum neurophysics extendable to describing subatomic reality. Beyond informing our appreciation of mechanisms generating sympathetic oscillations, Mayer waves may constitute an intrinsic property of neurons extant throughout the cerebrum, brainstem, and spinal cord or reflect an emergent property of interactions between arteriogenic and neuronal oscillations.

Mechanisms underlying the generation of autonomorespiratory coupling amongst the respiratory central pattern generator, sympathetic oscillators, and cardiovagal premotoneurons

“…The respiratory rhythm (Anderson et al, 2016;Anderson and Ramirez, 2017;Ghali, 2019c;Morgado-Valle and Beltran-Parrazal, 2017;Ramirez and Baertsch, 2018) and pattern Marchenko et al, 2016;Ramirez and Baertsch, 2018;Smith et al, 2009), sympathetic oscillations (Ghali, 2017a(Ghali, , 2019b, and cardiovagal premotoneuronal activity (Baekey et al, 2010;Bishop, 1974) are generated by distinct, though overlapping, networks residing chiefly within the metencephalon and myelencephalon (Ghali, 2017a(Ghali, ,b,c, 2019aMarchenko et al, 2016;Molkov et al, 2017) and powerfully modulated by descending synaptic inputs from the cerebrum (Antal, 1985), hippocampus (Ruit and Neafsey, 1988), amygdala (Lacuey et al, 2019), thalamus (Ogundele et al, 2017), hypothalamus (Fukushi et al, 2019), midbrain (Ghali and Ghali, 2020), and cerebellum (Horn and Waldrop, 1997;Schmid et al, 1988;Subramanian and Holstege, 2014). The widespread presence of autonomorespiratory coupling, manifest as baroreceptor and sympathetic modulation of neural respiratory activity (Baekey et al, 2010;Bishop, 1974;Lindsey et al, 1998), respirophasic modulation of sympathetic discharge (Haselton and Guyenet, 1989;Mandel and Schreihofer, 2006;McAllen, 1987;Molkov et al, 2017), and ambiguual cardiovagal premotoneurons (Dergacheva et al, 2010), and crossmodal modulation between sympathetic and parasympathetic outflows evidence coordinate inp...…”

“…Propriospinal microcircuit oscillators constituting emergently dynamic networks generate the respiratory rhythm and pattern (Figs. 1-3) (Ghali and Ghali, 2020), sympathetic oscillations (Figs. 4 and 5) (Barman, 2020), and cardiovagal premotoneuronal activity (Figs.…”

“…Neural and hemodynamic variability spectra exhibit high, low, and very-low-frequency oscillations Julien, 2006;Porta et al, 2018;Schweitzer, 1945;Ursino et al, 1992), constituting a mathematically interrogable set of phenomena (Seydnejad and Kitney, 2001) informing mechanisms generating sympathorespiratory modulation amongst and between disparate central oscillators (Ghali and Ghali, 2020). Stephan Hales initially reported oscillatory variability in the crural arterial pressure of a bound mare in 1733 (Hales, 1987).…”

“…These results imply chronic intermittent hypoxia-mediated genesis of late-expiratory synchronous bursting in abdominal and sympathetic neurograms could be mediated by coordinate synaptic inputs conveyed by chemosensitive glutamatergic retrotrapezoid nucleus units and parafacial respiratory group pre-inspiratory oscillators or neurosynaptic coupling of Bötzinger complex decrementing post-inspiratory and augmenting late-expiratory neurons and rostral ventrolateral medullary propriobulbar interneuronal microcircuit oscillators and presympathetic bulbospinal units (Molkov et al, 2014;Zoccal et al, 2008). Enhanced Bötzinger complex and rostral ventrolateral medullary neuronal spiking may express the composite influences of enhanced synaptic drive conveyed from the retrotrapezoid nucleus and parafacial respiratory group, sensitization of metencephalic and myelencephalic chemoreceptors by peripheral chemoreceptor inputs (Guyenet et al, 2019), or blunted inhibitory drive from Bötzinger complex postinspiratory neurons , compromised by hypoxic step reduction of the subpopulation of functionally active GABA and glycine receptor modulated neurosynaptic interactions (see Ghali and Ghali (2020)). These neuroplasticity mechanisms may utilize serotonergic (Mulkey et al, 2007) or purinergic (Mulkey et al, 2006) neuron transduction or be generated by oxidative stress.…”

The Cranial Bowl in the New Millennium and Sutherland's Legacy for Osteopathic Medicine: Part 1

“…Furthermore, this oscillation is not equal between the two hemispheres and can be influenced by the patient's emotional status [ 36 ]. Another known and measurable oscillation are those of Mayer (0.1 Hz), but its nature remains not understood and doubtful; these oscillations are probably related to autonomic nervous activity and the displacements of interstitial fluids [ 37 ]. Mayer oscillations can also be recorded in the spinal cord, probably with the same reasons hypothesized for the central nervous system [ 38 ].…”