Mono- and polysynaptic drive of oscillatory firing alpha 1 (FF) and alpha 2-motoneurons (FR) in a patient with spinal cord lesion.
Single-nerve fibre action potentials (APs) were recorded extracellularly from lower sacral nerve roots of patients with spinal cord lesions (paraplegics), and simultaneous single-fibre impulse patterns of alpha 1 (FF) and alpha 2-motoneurons (FR) and primary and secondary muscle spindle afferents were analyzed. An alpha 1-motoneuron was activated in a time-locked manner by a primary spindle afferent fibre to fire oscillatory with an oscillation period of 110 to 140 ms. The distribution width for the time-locking (phase) was approx. 3 ms, which is interpreted as monosynaptic activation. A phase-correlated firing of a secondary muscle spindle afferent fibre gave rise to an additional oscillation period of the oscillatory firing alpha 1-motoneuron, when the primary fibre ceased firing. The phase distribution width was approx. 80 ms, and therefore indicates polysynaptic drive. The drive of the oscillatory firing alpha 1-motoneuron thus included a monosynaptic from a primary and a polysynaptic activation from a secondary muscle spindle afferent fibre. An alpha 2-motoneuron was simultaneously activated to fire oscillatory by a different secondary spindle afferent fibre. The phase distribution width between them was approx. 120 ms, which indicates polysynaptic drive. The alpha 1 and alpha 2-motoneurons fired in the occasional firing mode and in the transient and continuous oscillatory firing mode. Upon touch, pin-prick and bladder and anal catheter pulling, the alpha 1-motoneuron changed its firing rate more quickly than did the alpha 2-motoneuron. Thus, the alpha 1-motoneuron fired more dynamically than did the alpha 2-motoneuron. Synchronous oscillatory firing of the alpha 1 and alpha 2-motoneurons occurred transiently during pin-pricking. It is discussed that transient synchronization of oscillatory firing motoneurons points to relative coordination of self-organized oscillatory firing motoneuronal networks to generate locomotion and other integrative functions. It is further discussed that loss of specific properties of spinal oscillators following spinal cord lesion may give rise to pathologic synchronization, and in this way to disorders in movement.
Schalow
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Department of Clinical Research, Swiss Paraplegic Centre Nottwil, Switzerland.
Zäch
G A
GA
D000200:Action Potentials / Q000502:physiology; D000344:Afferent Pathways / Q000503:physiopathology; D006801:Humans; D008959:Models, Neurological; D009046:Motor Neurons / Q000502:physiology*; D009412:Nerve Fibers / Q000502:physiology; D009991:Oscillometry; D010264:Paraplegia / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000503:physiopathology*; D013126:Spinal Nerve Roots / Q000503:physiopathology; D013569:Synapses / Q000502:physiology*; D013997:Time Factors; D001743:Urinary Bladder / Q000294:innervation / Q000503:physiopathology