1. The effects of stimulating hindlimb extensor nerves (100‐200 ms trains, 100 Hz, < or = 2 times threshold) during the flexor and extensor phases of the locomotor step cycle were analysed in the decerebrate, paralysed cat during fictive locomotion evoked by stimulation of the mesencephalic locomotor region. 2. Stimulation during extension of either the medial gastrocnemius (MG), lateral gastrocnemius‐soleus (LGS) or plantaris (Pl) nerves was equally effective in increasing the duration and amplitude of electroneurogram (ENG) activity recorded in ipsilateral ankle, knee and hip extensor nerves. Enhancement of extensor ENG activity could be evoked with near threshold stimulation intensity and appeared within 10‐40 ms of the onset of ankle extensor nerve stimulation. Stimulation of anterior biceps during extension occasionally evoked a modest increase in the duration of activity of hip, knee and ankle extensors. Stimulation of quadriceps during extension enhanced the activity of proximal extensors and soleus, but inhibited other ankle extensors. 3. Selective activation of ankle extensor Ia spindle afferents by muscle stretch also enhanced ipsilateral extension. It is argued that both muscle spindle and tendon organ afferents can contribute to the increase in extensor nerve activity evoked by group I stimulation intensity during fictive locomotion. 4. During flexion, stimulation of either the MG, Pl or LGS nerves at group I strength terminated on‐going activity in ipsilateral flexors and initiated a burst of activity in ipsilateral hip, knee and ankle extensors, i.e. reset the step cycle to extension. 5. Low strength stimulation of the mixed muscle and cutaneous nerve innervating the plantar aspect of the foot produced extension enhancement and resetting similar to that evoked by group I muscle afferent stimulation. Stimulation of the cutaneous nerve supplying the dorsal aspect of the foot during extension enhanced extensor activity, and during flexion, enhanced the activity of flexors. 6. The effects reported here during fictive locomotion may also occur during overground locomotion with natural activation of group I muscle spindle and tendon organ afferents. Extensor spindle and tendon organ afferents may thus serve as an excitatory reflex system helping to shape the amplitude, duration and timing of ipsilateral extensor activity. Increased or unexpected activation of group I ankle extensor afferents or plantar foot afferents during locomotion could also compensate for increased loading of the limb.

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This article provides a perspective on major innovations over the past century in research on the spinal cord and, specifically, on specialized spinal circuits involved in the control of rhythmic locomotor pattern generation and modulation. Pioneers such as Charles Sherrington and Thomas Graham Brown have conducted experiments in the early twentieth century that changed our views of the neural control of locomotion. Their seminal work supported subsequently by several decades of evidence has led to the conclusion that walking, flying, and swimming are largely controlled by a network of spinal neurons generally referred to as the central pattern generator (CPG) for locomotion. It has been subsequently demonstrated across all vertebrate species examined, from lampreys to humans, that this CPG is capable, under some conditions, to self-produce, even in absence of descending or peripheral inputs, basic rhythmic, and coordinated locomotor movements. Recent evidence suggests, in turn, that plasticity changes of some CPG elements may contribute to the development of specific pathophysiological conditions associated with impaired locomotion or spontaneous locomotor-like movements. This article constitutes a comprehensive review summarizing key findings on the CPG as well as on its potential role in Restless Leg Syndrome, Periodic Leg Movement, and Alternating Leg Muscle Activation. Special attention will be paid to the role of the CPG in a recently identified, and uniquely different neurological disorder, called the Uner Tan Syndrome.

1. This study examines the effects of electrical stimulation of hindlimb flexor nerves on the fictive locomotion pattern. Locomotion was initiated by stimulation of the mesencephalic locomotor region in the decerebrate paralysed cat and monitored by recording the electroneurogram from selected hindlimb flexor and extensor muscle nerves. Flexor nerves were stimulated using short trains (20-50 stimuli at 100 Hz) during either the flexor or the extensor phase of the fictive locomotor cycle. 2. Stimulation of tibialis anterior (TA), posterior biceps and semitendinosus (PBSt) or sartorius (Sart) nerves at 5 times threshold (T) during the flexor phase of the fictive locomotor cycle terminated on-going activity in flexor nerves and initiated activity in extensors. Thus, flexor nerve stimulation during flexion shortened the locomotor cycle by resetting to extension. The failure of lower intensity (2T) stimulation of PBSt or Sart nerves to reset the step cycle to extension suggests that group II afferents are responsible for these actions.Resetting evoked by 2 T stimulation of the TA nerve may be due to a high proportion of group II afferents with low electrical threshold. 3. During extension, stimulation of TA and PBSt nerves at 5Tdid not perturb the locomotor rhythm whereas Sart stimulation prolonged the locomotor cycle. 4. Stimulation of cutaneous or knee joint afferents failed to produce effects similar to those evoked by stimulation of flexor muscle nerves at group II strength. These findings are at odds with those obtained elsewhere in the acute spinal, DOPA fictive locomotion preparation. The possibility that group II resetting during fictive locomotion is not mediated by flexion reflex pathways but by previously unknown pathways released in the present preparation is discussed. 5. Since many of the flexor afferents recruited by 5T electrical stimulation are the lengthsensitive group II fibres, spindle secondaries may act to regulate the duration and onset of flexor and extensor activity during real locomotion. The resetting from flexion to extension also suggests that unexpected or enhanced activity of flexor secondaries during swing would promote a switch of the step cycle to stance.