title: Peripheral axon caliber and conduction velocity are decreased after burn injury in mice.
abstract: Peripheral neuropathies are reported to arise as a result of the systemic inflammatory response produced by a full-thickness cutaneous burn injury. This study was designed to characterize the magnitude and time course of functional and morphological changes in peripheral axons that arise after a full-thickness dermal burn injury in an animal model. A 20% body surface area (20% BSA) full-thickness dermal burn was applied to the back of C57BL6 female mice. Longitudinal H- and M-wave recordings were used to determine the conduction velocities (CV) of large myelinated motor and sensory axons in the tibial nerve of sham control and burn-injured mice. Motor CVs were significantly reduced from 6 h to 28 days after the burn, and sensory CVs were significantly reduced from 7 to 14 days after the burn. Morphological evaluation also showed that the mean caliber of large axons in tibial nerves and L5 ventral and dorsal roots in burned mice was significantly decreased. The results demonstrate that both functional and morphological deficits may be produced in peripheral nerve axons at sites well removed from a full-thickness dermal burn injury. The neural deficits may contribute to changes in neuromuscular transmission and the development of limb and respiratory muscle weakness that also accompany burn injury.
authors.affiliation: Department of Physiology and Membrane Biology, School of Medicine, University of California, One Shields Avenue, Davis, California 95616, USA.
authors.forename: Haruki
authors.initials: H
authors.lastname: Higashimori
authors.forename: Thomas P
authors.initials: TP
authors.lastname: Whetzel
authors.forename: Tamara
authors.initials: T
authors.lastname: Mahmood
authors.forename: Richard C
authors.initials: RC
authors.lastname: Carlsen
mesh_terms: D000818:Animals; D001369:Axons / Q000473:pathology* / Q000502:physiology / Q000648:ultrastructure; D002056:Burns / Q000150:complications*; D048429:Cell Size; D020405:Dermis / Q000293:injuries / Q000503:physiopathology; D004195:Disease Models, Animal; D004558:Electric Stimulation; D005260:Female; D006181:H-Reflex / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D009046:Motor Neurons / Q000473:pathology* / Q000648:ultrastructure; D009431:Neural Conduction / Q000502:physiology*; D009475:Neurons, Afferent / Q000473:pathology / Q000648:ultrastructure; D010523:Peripheral Nervous System Diseases / Q000209:etiology* / Q000473:pathology* / Q000503:physiopathology; D013979:Tibial Nerve / Q000473:pathology* / Q000503:physiopathology; D014855:Wallerian Degeneration / Q000209:etiology / Q000473:pathology / Q000503:physiopathology