Neuroscience 2005 Abstract
| Presentation Number: | 610.20 |
|---|---|
| Abstract Title: | Mobilization of calcium-dependent protein kinase C by concurrent activity and serotonin in <i>Aplysia</i> sensory neurons. |
| Authors: |
Leal, K.*1
; Abi-Farah, C.4
; Zhao, Y.2,3
; Martin, K. C.2,3
; Sossin, W. S.4
; Klein, M.1,3
1Physiological Science, UCLA, Los Angeles, CA 2Psychiatry & Biobehav. Sci., UCLA, Los Angeles, CA 3Brain Research Inst., UCLA, Los Angeles, CA 4PQ, 621 Charles Young Dr. S., 90095, |
| Primary Theme and Topics |
Neural Excitability, Synapses, and Glia: Cellular Mechanisms - Synaptic Plasticity -- Short-term plasticity |
| Secondary Theme and Topics | Cognition and Behavior<br />- Animal Cognition and Behavior<br />-- Learning and memory: Invertebrates |
| Session: |
610. Short-Term Plasticity II Poster |
| Presentation Time: | Tuesday, November 15, 2005 11:00 AM-12:00 PM |
| Location: | Washington Convention Center - Hall A-C, Board # E55 |
| Keywords: | SYNAPTIC PLASTICITY, LEARNING AND MEMORY, NEUROMODULATION, NEUROIMAGING |
Behavioral sensitization in the mollusk Aplysia is mediated in part by serotonin (5HT). 5HT facilitates transmission at sensorimotor synapses by mobilizing protein kinases A and C (PKC). Imaging experiments show that 5HT translocates the non-calcium-dependent PKC isoform Apl-II, but not the calcium-dependent Apl-I, from cytosol to membranes in living sensory neurons (Zhao et al., SFN abst., 2004). Consistent with this difference, introduction of a dominant negative form of Apl-II, but not of Apl-I, into sensory neurons inhibits 5HT-induced facilitation under some conditions.
To measure Apl-I tranlsocation we used a fluorescent Apl-I-EGFP construct. In SF9 cells only very high concentrations of diacylglycerol (DAG) translocated Apl-I, while low concentrations translocated Apl-II. However, calcium greatly decreased the requirement for DAG, suggesting that Apl-I could be a sensor of the combination of DAG and calcium. We tested this hypothesis by imaging Apl-I-EGFP expressed in sensory neurons.
The cellular distribution of Apl-I-EGFP was not affected by impalement with an intracellular electrode or by firing of action potentials. Application of 5HT was also ineffective. However, electrical stimulation in the presence of 5HT resulted in accumulation of Apl-I-EGFP at the plasma membrane and its reduction in the cytosol, consistent with translocation. Cessation of firing reversed these changes, and translocation could be induced repeatedly by firing in the presence of 5HT. Together with earlier work showing that concurrent firing and application of 5HT cause an intermediate-term form of facilitation that is maintained by persistent activity of PKC (Sutton et al., J. Neurosci. 24:3600), our findings suggest that mobilization of Apl-I contributes to intermediate-term facilitation and the consequent behavioral sensitization.
To measure Apl-I tranlsocation we used a fluorescent Apl-I-EGFP construct. In SF9 cells only very high concentrations of diacylglycerol (DAG) translocated Apl-I, while low concentrations translocated Apl-II. However, calcium greatly decreased the requirement for DAG, suggesting that Apl-I could be a sensor of the combination of DAG and calcium. We tested this hypothesis by imaging Apl-I-EGFP expressed in sensory neurons.
The cellular distribution of Apl-I-EGFP was not affected by impalement with an intracellular electrode or by firing of action potentials. Application of 5HT was also ineffective. However, electrical stimulation in the presence of 5HT resulted in accumulation of Apl-I-EGFP at the plasma membrane and its reduction in the cytosol, consistent with translocation. Cessation of firing reversed these changes, and translocation could be induced repeatedly by firing in the presence of 5HT. Together with earlier work showing that concurrent firing and application of 5HT cause an intermediate-term form of facilitation that is maintained by persistent activity of PKC (Sutton et al., J. Neurosci. 24:3600), our findings suggest that mobilization of Apl-I contributes to intermediate-term facilitation and the consequent behavioral sensitization.
Supported by NINDS, CIHR and the W.M. Keck Foundation
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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