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Introduction: The rat tail exhibits functional impairment after cauda equina injury. Our goal was to better understand the innervation and roles of muscles that control the tail., Methods: Adult rats received either: (1) ventral root injury; (2) caudales nerve injury; or (3) mapping of sacrococcygeal myotomes. Activation of small muscles within the tail itself (intrinsics) was compared with that of larger lumbosacral muscles acting on the tail (extrinsics). Behavioral testing of tail movement was done 1 week later., Results: Rats that received ventral root injury exhibited multiple behavioral deficits, whereas rats with injury to caudales nerves maintained more fully preserved tail movement. Mapping studies revealed much broader overlap of myotomes for extrinsic muscles., Conclusions: Extrinsic tail muscles play a greater role in tail movement in the rat than their intrinsic counterparts and are innervated by multiple neurological segments. These findings have major implications for future research on cauda equina injury., (© 2014 Wiley Periodicals, Inc.)

Prolonged hand-transmitted vibration exposure in the workplace has been recognized for almost a century to cause neurodegenerative and vasospastic disease. Persistence of the diseased state for years after cessation of tool use is of grave concern. To understand persistence of vibration injury, the present study examined recovery of nerve conduction velocity and structural damage of myelinated axons in a rat tail vibration model. Both 7 and 14 days of vibration (4 h/day) decreased conduction velocity. The decrease correlated directly with the increased percentage of disrupted myelinated axons. The total number of myelinated axons was unchanged. During 2 months of recovery, conduction velocity returned to control level after 7-day vibration but remained decreased after 14-day vibration. The rat tail model provides insight into understanding the persistence of neural deficits in hand-arm vibration syndrome.

The effect of long-term (40 min) high frequency stimulation (143 Hz) of sensory-motor tail nerves was studied in normal and in streptozotocin-diabetic rats. The study comprised a 6-week period, repeating the test at 2-week intervals. In the initial (prediabetic) study, single experiments showed a mild depression of the peak-to-peak amplitude during high frequency stimulation, which reversed completely during a subsequent rest period. In normal rats, the amplitude depression was unchanged in repeated tests over a 6-week period. Diabetic rats showed a greater amplitude depression during high frequency stimulation. The difference was statistically significant after 2 weeks, but showed no further change at subsequent tests. The greater decrease in the amplitude in diabetic rats may reflect a depression of the axon membrane function, which may be the functional correlate to the inhibition of the Na/K ATPase activity in diabetes, described by others. Monitoring of the axon membrane functional capacity may have clinical implications in the control of peripheral neuropathies.