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Journal of Experimental Biology, Vol 190, Issue 1 217-238, Copyright © 1994 by Company of Biologists
JOURNAL ARTICLES |
AL Clatworthy and ET Walters
Department of Physiology and Cell Biology, University of Texas Medical School at Houston 77225.
Long-term effects of nerve injury on electrophysiological properties were compared in two populations of mechanosensory neurones in Aplysia californica: the J and K clusters in the cerebral ganglia and the VC clusters in the pleural ganglia. Following crush of cerebral nerves containing their axons, the cerebral J/K sensory neurones showed long-term changes that were quite similar to alterations previously described in the VC sensory neurones after either axonal injury or aversive learning. These changes include synaptic facilitation, an increase in soma excitability and spike duration, and a decrease in spike threshold and afterhyperpolarization. In addition, simultaneous crush of both the cerebral and pedal nerves in the same animals produced alterations in the cerebral J/K sensory neurones and pleural VC sensory neurones that were virtually identical. The incidence of hyperexcitability was the same in cerebral J/K and pleural VC sensory neurones when all their axons were crushed, even though the former population includes many neurones that probably have appetitive functions while the latter population appears to be made up exclusively of neurones with defensive functions. Long-term plasticity in both sensory populations failed to occur when nerves lacking axons of the tested neurones were crushed, even when the crush site was very close to the somata of the sensory neurones. This axonal specificity argues against a role for delayed activation of facilitatory interneurones in triggering the plasticity. Several observations are consistent with a triggering role for either (1) intracellular signals released directly by axonal injury or (2) extracellular signals released locally by other axons or injured support cells, or by immunocytes attracted to the injured site.
This article has been cited by other articles:
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S. S. Rubakhin, L. Li, T. P. Moroz, and J. V. Sweedler Characterization of the Aplysia californica Cerebral Ganglion F Cluster J Neurophysiol, March 1, 1999; 81(3): 1251 - 1260. [Abstract] [Full Text] [PDF]
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L. J. Cleary, W. L. Lee, and J. H. Byrne Cellular Correlates of Long-Term Sensitization in Aplysia J. Neurosci., August 1, 1998; 18(15): 5988 - 5998. [Abstract] [Full Text] [PDF]
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M. Povelones, K. Tran, D. Thanos, and R. T. Ambron An NF-kappa B-Like Transcription Factor in Axoplasm is Rapidly Inactivated after Nerve Injury in Aplysia J. Neurosci., July 1, 1997; 17(13): 4915 - 4920. [Abstract] [Full Text] [PDF]
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P. A. Illich and E. T. Walters Mechanosensory Neurons Innervating Aplysia Siphon Encode Noxious Stimuli and Display Nociceptive Sensitization J. Neurosci., January 1, 1997; 17(1): 459 - 469. [Abstract] [Full Text] [PDF]
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 K K Fitzgerald and T J Carew Multiple forms of facilitation produced by aversive tentacular stimuli in cerebral ganglion sensory neurons of Aplysia. Learn. Mem., January 1, 1997; 3(5): 376 - 388. [Abstract] [PDF]
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R. T. Ambron, X.-P. Zhang, J. D. Gunstream, M. Povelones, and E. T. Walters Intrinsic Injury Signals Enhance Growth, Survival, and Excitability of Aplysia Neurons J. Neurosci., December 1, 1996; 16(23): 7469 - 7477. [Abstract] [Full Text] [PDF]
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