QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, November 17, 2004, 24(46):10393-10401; doi:10.1523/JNEUROSCI.2329-04.2004

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (12) Citing Articles via Google Scholar Google Scholar Articles by Weragoda, R. M. S. Articles by Walters, E. T. Search for Related Content PubMed PubMed Citation Articles by Weragoda, R. M. S. Articles by Walters, E. T. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information Memory Hazardous Substances DB POTASSIUM

 Previous Article  |  Next Article 

Behavioral/Systems/Cognitive
Memory-Like Alterations in Aplysia Axons after Nerve Injury or Localized Depolarization

Ramal M. S. Weragoda, Elisa Ferrer, and Edgar T. Walters

Department of Integrative Biology and Pharmacology, University of Texas-Houston Medical School, Houston, Texas 77030

Adaptive, long-term alterations of excitability have been reported in dendrites and presynaptic terminals but not along axons. Persistent enhancement of axonal excitability has been described in proximal nerve stumps at sites of nerve section in mammals, but this hyperexcitability is considered a pathological derangement important only as a cause of neuropathic pain. Identified neurons in Aplysia were used to test the hypothesis that either axonal injury or the focal depolarization that accompanies axonal injury can trigger a local decrease in action potential threshold [long-term hyperexcitability (LTH)] having memory-like properties. Nociceptive tail sensory neurons and a giant secretomotor neuron, R2, exhibited localized axonal LTH lasting 24 hr after a crush of the nerve or connective that severed the tested axons. Axons of tail sensory neurons and tail motor neurons, but not R2, displayed similar localized LTH after peripheral depolarization produced by 2 min exposure to elevated extracellular [K⁺]. Neither the induction nor expression of either form of LTH was blocked by saline containing 1% normal [Ca²⁺] during treatment or testing. However, both were prevented by local application of the protein synthesis inhibitors anisomycin or rapamycin. The features of (1) long-lasting alteration by localized depolarization, (2) restriction of alterations to intensely depolarized regions, and (3) dependence of the alterations on local, rapamycin-sensitive protein synthesis are shared with synaptic mechanisms considered important for memory formation. This commonality suggests that relatively simple, accessible axons may offer an opportunity to define fundamental plasticity mechanisms that were important in the evolution of memory.

Key words: hyperexcitability; memory; action potential threshold; sensitization; protein synthesis; axotomy; neuropathic pain

---

Received June 14, 2004; revised October 6, 2004; accepted October 7, 2004.

This article has been cited by other articles:

				K. K. Kunjilwar, H. M. Fishman, D. J. Englot, R. G. O'Neil, and E. T. Walters Long-Lasting Hyperexcitability Induced by Depolarization in the Absence of Detectable Ca2+ Signals J Neurophysiol, March 1, 2009; 101(3): 1351 - 1360. [Abstract] [Full Text] [PDF]

				S. S. Bedi, D. Cai, and D. L. Glanzman Effects of Axotomy on Cultured Sensory Neurons of Aplysia: Long-Term Injury-Induced Changes in Excitability and Morphology Are Mediated by Different Signaling Pathways J Neurophysiol, December 1, 2008; 100(6): 3209 - 3224. [Abstract] [Full Text] [PDF]

				T. J. Price, M. H. Rashid, M. Millecamps, R. Sanoja, J. M. Entrena, and F. Cervero Decreased Nociceptive Sensitization in Mice Lacking the Fragile X Mental Retardation Protein: Role of mGluR1/5 and mTOR J. Neurosci., December 19, 2007; 27(51): 13958 - 13967. [Abstract] [Full Text] [PDF]

				R. M. S. Weragoda and E. T. Walters Serotonin Induces Memory-Like, Rapamycin-Sensitive Hyperexcitability in Sensory Axons of Aplysia That Contributes to Injury Responses J Neurophysiol, September 1, 2007; 98(3): 1231 - 1239. [Abstract] [Full Text] [PDF]

				X. Guan and G. A. Clark Essential Role of Somatic and Synaptic Protein Synthesis and Axonal Transport in Long-Term Synapse-Specific Facilitation at Distal Sensorimotor Connections in Aplysia Biol. Bull., June 1, 2006; 210(3): 238 - 254. [Abstract] [Full Text] [PDF]

				X. Gasull, X. Liao, M. F. Dulin, C. Phelps, and E. T. Walters Evidence That Long-Term Hyperexcitability of the Sensory Neuron Soma Induced by Nerve Injury in Aplysia Is Adaptive J Neurophysiol, September 1, 2005; 94(3): 2218 - 2230. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help