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Four studies were conducted to delineate potential neural processes involved in retention of a peripherally induced postural asymmetry. In the first experiment, dorsal and ventral spinal root section following varying intervals of stimulation successfully abolished peripherally induced hindlimb asymmetry. Experiment 2 revealed that 50 min of ventral root stimulation, in the absence of central connection, was not effective in producing asymmetry persistence. In an attempt to more closely delineate the time parameters involved in peripherally induced asymmetry retention, Experiment 3 was conducted. Asymmetry was found to consistently outlast a spinal transection if 40 min of stimulation was given. Finally, possible modulatory higher brain center influences on the retention processes were demonstrated in Experiment 4. Asymmetry persistence was consistently observed in animals that received 10, 20, 30, 40, or 50 min of hindlimb stimulation if 50 min were allowed to elapse between the onset of stimulation and spinal section. These results, when coupled with the findings of earlier studies, suggest an active involvement of spinal reflex centers in the fixation process. In addition, these studies indicate that the manner in which reflex activity is altered is not crucial as long as underlying time parameters are adhered to. Finally, the present studies demonstrate that higher center influences can modulate retention of a postural asymmetry in a complex manner.

Two methods were used to demonstrate retention of postural asymmetries after spinal cord section in adult rats. In the first preparation, postural asymmetries of the hindlimbs were induced by placing electrolytic lesions in the anterior cerebellum. Asymmetry was found to consistently outlast a spinal cord section if 45 min were allowed between brain lesion and cord section. A certain percentage of rats allowed 35 or 40 min also demonstrated the retention. In the second preparation, postural asymmetries induced by 45 min of direct hindlimb stimulation were also retained after spinal section. Rhizotomy prior to stimulation resulted in a lack of appreciable asymmetry upon termination of the stimulation. Finally, retention of a hindlimb-stimulation-induced asymmetry was observed in animals that underwent a spinal section prior to the stimulation. The present series of studies demonstrates that the "spinal fixation" phenomenon can be obtained by induction of postural alterations from central (cerebellar lesion) and peripheral (hindlimb stimulation) sources. In addition, results obtained from spinal animals indicate that retention of peripherally induced asymmetry is not crucially dependent on higher brain center activity but rather seems to be more dependent on long-term alterations that occur directly in the spinal reflex system.

Temporal parameters concerning retention of a stimulation-induced hindlimb flexion were investigated. After spinal transection, 60 rats received 10, 20, 30, 40, 45, or 50 min of hindlimb stimulation. Consistent persistence of flexion following stimulus cessation was observed in rats that were stimulated for at least 30 min. When the results ae compared with previous data, the spinalized rat shows a 10-min reduction in the critical time interval needed to consistently obtain poststimulation persistence of flexion.