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Mohammed, M. A. Y.

Publications and source records attributed to Mohammed, M. A. Y..

2 recordsLinked to original sources

Speed-Dependent Turning Strategies in Quadrupedal Locomotion: Insights from Computational Modeling

Quadrupedal animals like mice navigate their environments through complex coordination of neural signals and biomechanical movements, enabling stable and directed locomotion. While many computational models simplify this process by assuming left-right symmetrical body movements and focusing on straight-line paths, real animals rely heavily on asymmetrical body movements to execute turns and adjust speed effectively. This study builds upon a previously developed model of quadrupedal locomotion proposed by Molkov et al., 2024) in which forward movement of the body was driven by central neural interactions, biomechanics, and proprioceptive feedback. We extended this model to comparatively investigate possible mechanisms of steering by introducing three distinct asymmetrical strategies-body bending, lateral force application, and lateral limb shifting as well as their combinations-to explore their potential involvement in turning performance. By simulating these strategies across a walking speed range, we measured and compared their impact on turning curvature the sharpness of the turn) and limb coordination. The latter was quantified through ratios of duty factors representing the relative time that a limb spent in contact with the ground compared to its counterpart on the opposite side. Our findings reveal that each strategy excels at different speeds: body bending allows sharp turns at low speeds, lateral force is most effective at medium speeds, and lateral shifting performs best at higher speeds. Our results suggest that animals select or combine turning strategies based on their locomotor speed or adjust speed to use a specific strategy. We also show that the forelimbs consistently play a primary role in steering, while the hindlimbs adjust propulsion and stability in ways that depend on the specific turning strategy. These results provide valuable insights into how spinal circuits and mechanical asymmetries work together to produce flexible, adaptive movement patterns, offering a robust framework for understanding locomotion in both biological organisms and robotic systems designed to mimic such behaviors.

systems biology↗

Ionic Mechanisms Underlying Bistability in Spinal Motoneurons: Insights from a Computational Model

Spinal motoneurons are the final output of spinal circuits that engage skeletal muscles to generate motor behaviors. Many motoneurons exhibit bistable behavior, alternating between a quiescent resting state and a self-sustained firing mode, classically attributed to plateau potentials driven by persistent inward currents. This intrinsic property is important for normal movement control, but can become dysregulated, causing motor function deficits, like spasticity. Here we use a conductance-based single-compartment model, together with mouse spinal slice recordings,to investigate the ionic interactions underlying motoneuron bistability. We show that synergistic interactions among high-voltage-activated L-type Ca2+ current (ICaL), calcium-induced calcium release (CICR) and the Ca2+-activated non-specific cation current (ICAN) constitute a minimal mechanistic core that produces plateau potentials and bistable firing. Within this framework, the persistent sodium current (INaP) promotes plateau generation, in contrast to the Ca2+-dependent K+ current (IKCa) which opposes it. These results delineate ionic dependencies at the level of interactions rather than spatial localisation and provide a tractable basis for interpreting altered motoneuron excitability in disease. Key PointsO_LIWe investigated how spinal motoneurons, critical for skeletal muscle control, exhibit bistability, switching between quiet and self-sustained firing. This property stabilizes motor functions like postural control, and its dysregulation contributes to disorders such as spasticity. Using a single-compartment computational model and mouse spinal slice recordings, we explored the ionic interactions driving bistability. C_LIO_LIOur findings reveal that a calcium-activated cation non-specific current and calcium-induced calcium release form a core mechanism supporting the plateau depolarization essential for bistable firing. Within this framework, the persistent sodium current facilitates plateau generation, while the calcium-dependent potassium current counteracts it. Pharmacological manipulations in slices yielded results consistent with these current roles. C_LIO_LIOur study delineates the ionic dependencies of motoneuron bistability based on interactions, not spatial location. This offers a concise framework for interpreting excitability changes observed in normal conditions and following spinal cord injury, providing valuable insights into motor function and neurological disorders. C_LI

neuroscience↗