期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1990
卷号：87
期号：5
页码：2036-2039
DOI：10.1073/pnas.87.5.2036
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：The defensive tail-withdrawal reflex of Aplysia californica, mediated by identified sensory neurons in pleural ganglia that form synapses on motor cells in pedal ganglia, can be sensitized by stimulating the animal with electric shock. The neurophysiological basis of this simple form of learning is thought to be the increased release of transmitter by the sensory neurons. Earlier work has focused on cAMP-dependent protein phosphorylation as the cause of the presynaptic facilitation underlying short-term sensitization. Using physiological concentrations of Mg2+ during fractionation, we now find that, independent from cAMP, protein kinase C is translocated in sensory neurons by sensitizing stimuli. Translocation occurred after behavioral training of the animal and after application to isolated ganglia of serotonin or phorbol esters. Taken together with the neurophysiological evidence presented in the accompanying paper that phorbol esters can produce the facilitation, these biochemical results suggest that protein kinase C plays a role in producing the presynaptic facilitation that underlies short-term sensitization and dishabituation of defensive reflexes.
