Morphological and physiological survival of goldfish Mauthner axons isolated from their somata by spinal cord crush.
Axon segments isolated from their somata degenerate within days or months depending on species and neuronal type. To better understand the time course of morphological and physiological changes associated with degeneration of axon segments of vertebrate central neurons, we have studied the goldfish Mauthner axon (M-axon) when it has been separated from its soma by spinal cord crush. M-axon segments survive morphologically for at least 77 days at 14 degrees C. Cross-sectional areas of isolated M-axon segments (measured 25-30 mm caudal to the wound site at postoperative days 64 and 77) were greater than those of control axons at the same level. Sheath areas did not change. Electron microscopic observations at the same spinal cord location indicated no clear changes in the configuration or number of neurofilaments or any other organelle. M-axon segments studied morphologically after 87 postoperative days had all degenerated. Mauthner axon segments were capable of conducting action potentials and eliciting ipsilateral EMG responses. Repetitive firing of the M-axon segments elicited EMG responses that fatigued more easily and remained fatigued over a longer interval than did those of control axons. The long duration of M-axon segment survival is unusual in a vertebrate and may be due to the low temperature at which the experiments were conducted (14 degrees C) and/or temperature-independent factors. The increased susceptibility to synaptic depression, which has not reported previously, may represent an early sign of the degenerative process.
D000818:Animals; D001369:Axons / Q000473:pathology / Q000502:physiology; D002470:Cell Survival; D002490:Central Nervous System / Q000503:physiopathology*; D003530:Cyprinidae / Q000502:physiology*; D006054:Goldfish / Q000502:physiology*; D008526:Medulla Oblongata / Q000166:cytology*; D008854:Microscopy, Electron; D009431:Neural Conduction; D013119:Spinal Cord Injuries / Q000473:pathology / Q000503:physiopathology*