What determines how we move in the world? Motor neuroscience often focusses either on intrinsic rhythmical properties of motor circuits or extrinsic sensorimotor feedback loops. Here we show that the interplay of both intrinsic and extrinsic dynamics is required to explain the intermittency observed in continuous tracking movements. Using spatiotemporal perturbations in humans, we demonstrate that apparently discrete submovements made 2–3 times per second reflect constructive interference between motor errors and continuous feedback corrections that are filtered by intrinsic circuitry in the motor system. Local field potentials in monkey motor cortex revealed characteristic signatures of a Kalman filter, giving rise to both low-frequency cortical cycles during movement, and delta oscillations during sleep. We interpret these results within the framework of optimal feedback control, and suggest that the intrinsic rhythmicity of motor cortical networks reflects an internal model of external dynamics, which is used for state estimation during feedback-guided movement.Editorial note: This article has been through an editorial process in which the authors decide how to respond to the issues raised during peer review. The Reviewing Editor's assessment is that all the issues have been addressed (<xref ref-type="decision-letter" rid="SA1">see decision letter</xref>).
Key points The first indirect (I) corticospinal volley from stimulation of the motor cortex consists of two parts: one that originates from infragranular layer 5 and a subsequent part with a delay of 0.6 ms to which supragranular layers contribute. Non‐invasive probing of these two parts was performed in humans using a refined electrophysiological method involving transcranial magnetic stimulation and peripheral nerve stimulation. Activity modulation of these two parts during a sensorimotor discrimination task was consistent with previous results in monkeys obtained with laminar recordings. Abstract Circuits in superficial and deep layers play distinct roles in cortical computation, but current methods to study them in humans are limited. Here, we developed a novel approach for non‐invasive assessment of layer‐specific activity in the human motor cortex. We first conducted brain slice and in vivo experiments on monkey motor cortex to investigate the output timing from layer 5 (including corticospinal neurons) following extracellular stimulation. Neuron responses contained cyclical waves. The first wave was composed of two parts: the earliest part originated only from stimulation of layer 5; after 0.6 ms, stimuli to superficial layers 2/3 could also contribute. In healthy humans we then assessed different parts of the first corticospinal volley elicited by transcranial magnetic stimulation (TMS), by interacting TMS with stimulation of the median nerve generating an H‐reflex. By adjusting the delay between stimuli, we could assess the earliest volley evoked by TMS, and the part 0.6 ms later. Measurements were made while subjects performed a visuo‐motor discrimination task, which has been previously shown in monkey to modulate superficial motor cortical cells selectively depending on task difficulty. We showed a similar selective modulation of the later part of the TMS volley, as expected if this part of the volley is sensitive to superficial cortical excitability. We conclude that it is possible to segregate different cortical circuits which may refer to different motor cortex layers in humans, by exploiting small time differences in the corticospinal volleys evoked by non‐invasive stimulation.
Sequential firing of neurons during sleep is thought to play a role in the consolidation of learning. However, direct evidence for such sequence replay is limited to only a few brain areas and sleep states mainly in rodents. Using a custom-designed wearable neural data logger and chronically implanted electrodes, we made long-term recordings of neural activity in the primary motor cortex of two female nonhuman primates during free behavior and natural sleep. We used the local field potential (LFP) spectrogram to characterize sleep cycles, and examined firing rates, correlations, and sequential firing of neurons at different frequency bands through the cycle. Slow-wave sleep (SWS) was characterized by low neural firing rates and high synchrony, reflecting slow oscillations between cortical down and up states. However, the order in which neurons entered up states was similar to the sequence of neural activity observed at low frequencies during waking behavior. In addition, we found evidence of brief bursts of theta oscillation, associated with non-SWS states, during which neurons fired in strikingly regular sequential order phase-locked to the LFP. Theta sequences were preserved between waking and sleep, but appeared not to resemble the order of neural activity observed at lower frequencies. The sequential firing of neurons during slow oscillations and theta bursts may contribute to the consolidation of procedural memories during sleep. SIGNIFICANCE STATEMENT Replay of sequential neural activity during sleep is believed to support consolidation of daytime learning. Despite a wealth of studies investigating sequential replay in association with episodic and spatial memory, it is unknown whether similar sequences occur in motor areas during sleep. Within long-term neural recordings from monkey motor cortex, we found two distinct patterns of sequential activity during different phases of the natural sleep cycle. Slow-wave sleep was associated with delta-band sequences that resembled low-frequency activity during movement, while occasional brief bursts of theta oscillation were associated with a different order of sequential firing. Our results are the first report of sequential sleep replay in the motor cortex, which may play an important role in consolidation of procedural learning.
Based on the potential theory of incompressible flow and the energy method, a two-dimensional simply supported thin panel subjected to external forcing and uniform incompressible subsonic flow is theoretically modeled. The nonlinear cubic stiffness and viscous damper in the middle of the panel is considered. Transformation of the governing partial differential equation to a set of ordinary differential equations is performed through the Galerkin method. The stability of the fixed points of the panel system is analyzed. The regions of different motion types of the panel system are investigated in different parameter spaces. The rich dynamic behaviors are presented as bifurcation diagrams, phase-plane portraits, Poincaré maps and maximum Lyapunov exponents based on carefully numerical simulations.
The effects of alterations in intracellular calcium homeostasis on surface membrane excitability were investigated in resting Rana temporaria sartorius muscle. This was prompted by initial results from a fatiguing stimulation protocol study that demonstrated a fibre subpopulation in which action potential generation in response to a standard 1.5 V electrical stimulus failed despite mean membrane potentials [E (m), -69+/-2.3 mV (n=14)] compatible with spike firing in a control set of quiescent muscle fibres. Intracellular micro-electrode recordings showed a similar reversible loss of excitability, attributable to an increased threshold, despite only small (7.1+/-1.8 mV) positive changes in E (m) after approximately 60-min exposures to nominally 0 Ca(2+) Ringer solutions in which Ca(2+) was replaced by Mg(2+). This effect was not reproduced by addition of Mg(2+) to the Ringer solution and persisted under conditions of Cl(-) deprivation. The effects of three pharmacological agents, cyclopiazonic acid (CPA), caffeine and 4-chloro-m-cresol (4-CmC), each known to deplete store Ca(2+) and increase cytosolic Ca(2+) through contrasting mechanisms without influencing E (m), were then investigated. All three agents produced a more rapid, but nevertheless still reversible, loss of membrane excitability than in 0 Ca(2+) Ringer solution alone. This reduction in membrane excitability persisted in fibres studied in solutions containing a normal [Ca(2+)] following prior depletion of store Ca(2+) using CPA- and 4-CmC-containing solutions. These novel findings suggest that sarcoplasmic reticulum Ca(2+) content profoundly influences surface membrane excitability, thereby providing a potential mechanism by which spike firing fails in well-polarised fibres during fatigue.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.