Automatic postural responses are delayed by pyridoxine-induced somatosensory loss

Abstract

Pyridoxine given in large doses is thought to destroy selectively the large-diameter peripheral sensory nerve fibers, leaving motor fibers intact. This study examined the effects of pyridoxine-induced somatosensory loss on automatic postural responses to sudden displacements of the support surface in the standing cat. Two cats were trained to stand on four force plates mounted on a movable platform. They were given pyridoxine (350 mg/kg, i.p.) on 2 successive days (0 and 1). Electromyographic (EMG) activity was recorded from selected hindlimb muscles during linear ramp-and-hold platform displacements in each of 12 directions at 15 cm/sec. In control trials onset latencies of evoked activity in hindlimb flexor and extensor muscles ranged from 40 to 65 msec after the onset of platform acceleration. After injection the EMG latencies increased over days, becoming two to three times longer than controls by day 7. Excursions of the body center of mass (CoM) in the direction opposite to that of platform translation were significantly greater at day 7 compared with controls, and the time at which the CoM subsequently reversed direction was delayed. Both animals were ataxic from day 2 onward. Histological analysis of cutaneous and muscle nerves in the hindlimb revealed a significant loss of fibers in the group I range. Our results suggest that large afferent fibers are critical for the timing of automatic postural responses to ensure coordinated control of the body CoM and balance after unexpected disturbances of the support surface.

Fig. 1.

Representative averaged EMG activity of hindlimb muscles for cat Wo before (black) and on day 7 after pyridoxine (gray). The translation directions that are illustrated are those for which each muscle was activated maximally in the control condition. The dashed vertical line indicates the onset of platform acceleration. For muscles SEMP and LGAS the baseline EMG activity is indicated byhorizontal dotted lines to clarify initial burst onset. Under each trace, arrows indicate response onset during control trials and at day 7. GLUT, Gluteus medius;BFMM, middle biceps femoris; SRTA, anterior sartorius; SEMP, posterior semimembranosus;LGAS, lateral gastrocnemius. Inset shows coordinate reference for direction of translation.

Fig. 2.

A, Representative horizontal plane center of mass (CoM) trajectories for each cat in control (black) and postpyridoxine (gray) conditions for one selected direction (240°). For comparison, control and postpyridoxine trajectories are aligned to the same initial position (open circles). B, Amplitude of maximum initial displacement of the CoM from its origin (see region labeled Max Displ in A).C, Time of maximum displacement with respect to the onset of platform translation. Error bars indicate SE. **Significantly different from control values (p < 0.001).

Fig. 3.

Frequency versus diameter of all myelinated nerve fibers for saphenous (cutaneous) and medial gastrocnemius (mixed motor and sensory) nerves for both pyridoxine cats (gray) and one control (black). In each, the main plot shows absolute counts for diameters in 1 μm bins, and the inset at toprightshows cumulative frequency plots of the same data. The saphenous nerve was sampled 2 cm above the ankle and the gastrocnemius at 1 cm from its entry point to the muscle.