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J Neurophysiol 97: 1862-1867, 2007. First published January 3, 2007; doi:10.1152/jn.01230.2006
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Activity-Dependent Peptidergic Modulation of the Plateau-Generating Neuron B64 in the Feeding Network of Aplysia

Hae-Young Koh1,2 and Klaudiusz R. Weiss1

1Department of Neuroscience, Mount Sinai School of Medicine, New York, New York; and 2Center for Neural Science, Life Sciences Division, Korea Institute of Science and Technology, Seoul, Korea

Submitted 22 November 2006; accepted in final form 1 March 2007

Many behaviors display various forms of activity-dependent plasticity. An example of such plasticity is the progressive shortening of the duration of protraction phase of feeding responses of Aplysia that occurs when feeding responses are repeatedly elicited. A similar protraction-duration shortening is observed in isolated ganglia of Aplysia when feeding-like motor programs are elicited through a prolonged stimulation of the command-like neuron CBI-2. Here, we investigate a cellular mechanism that may underlie this activity-dependent shortening of protraction duration of feeding motor programs. CBI-2 contains two neuropeptides, CP2 and FCAP. Previous work showed that CP2 shortens protraction duration of CBI-2 elicited programs. We show here that the same is true for FCAP. We also show that both CP2 and FCAP modulated the biophysical properties of a plateau-generating neuron, B64, that plays an important role in terminating the protraction phase of feeding motor programs. We find that prestimulation of CBI-2, as well as superfusion of CP2 and FCAP, lowered the threshold for activation of the plateau potential in B64. The threshold-lowering actions of CBI-2 prestimulation were occluded by superfusion of FCAP and CP2. Furthermore, at elevated temperature, conditions under which peptide release is prevented in Aplysia, prestimulation of CBI-2 does not lower the plateau-potential threshold, whereas superfusion of CP2 and FCAP does. Our findings are consistent with the hypothesis that peptides released from CBI-2 lower the threshold for activation of plateau potential in B64, thereby contributing to the shortening of protraction duration when CBI-2 is repeatedly activated.


Address for reprint requests and other correspondence: K. R. Weiss, Department of Neuroscience, Mount Sinai School of Medicine, 1 Gustave Levy Place, New York, NY 10029 (E-mail: Klaudiusz.Weiss{at}mssm.edu)




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