Publication Date:
1991-08-16
Description:
Learning in the marine mollusk Aplysia has been associated with enhanced sensory function, expressed in mechanosensory neurons as (i) decreases in action potential threshold, accommodation, and afterhyperpolarization, and (ii) increases in action potential duration, afterdischarge, and synaptic transmission. These alterations also occur, with a delay, after sensory axons are injured under conditions in which synaptic transmission is severely reduced. The latency and specificity of injury-induced alterations indicate that induction signals are generated at the site of injury and conveyed centrally by axonal transport. Similarities in neuronal modifications support the hypothesis that some memory mechanisms evolved from mechanisms of injury-induced sensory compensation and repair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walters, E T -- Alizadeh, H -- Castro, G A -- AI11361/AI/NIAID NIH HHS/ -- MH38726/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1991 Aug 16;253(5021):797-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Cell Biology, University of Texas Medical School, Houston 77225.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1652154" target="_blank"〉PubMed〈/a〉
Keywords:
Action Potentials
;
Animals
;
Aplysia/anatomy & histology/*physiology
;
Axons/*physiology
;
Electric Stimulation
;
Learning/*physiology
;
Membrane Potentials
;
Nerve Crush
;
Neuronal Plasticity/*physiology
;
Synaptic Transmission
;
Time Factors
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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