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Updated: Aug 15, 2026

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Preparation of Aplysia Sensory-motor Neuronal Cell Cultures
Published on: June 8, 2009
Long-term heterosynaptic inhibition in Aplysia
P G Montarolo1, E R Kandel, S Schacher
1Howard Hughes Medical Institute, Columbia University, College of Physicians and Surgeons, New York, New York.
Nature
|May 12, 1988
Summary
The peptide Phe-Met-Arg-Phe-amide (FMRFamide) induces long-term synaptic depression in Aplysia
Area of Science:
- Neuroscience
- Cellular Neuroscience
- Synaptic Plasticity
Background:
- Synaptic transmission in Aplysia's gill withdrawal reflex exhibits short-term and long-term modulation.
- Short-term synaptic depression, lasting minutes, is induced by Phe-Met-Arg-Phe-amide (FMRFamide) via the arachidonic acid lipoxygenase pathway.
Purpose of the Study:
- To investigate the induction of long-term synaptic depression (LTD) in the Aplysia gill withdrawal reflex.
- To determine if FMRFamide can induce LTD and compare its characteristics to short-term depression and other modulatory pathways.
Main Methods:
- Utilized Aplysia cell culture to study the monosynaptic sensory-to-motor connection.
- Applied FMRFamide repeatedly over a 2-hour period to induce long-term changes.
- Investigated the effect of anisomycin, a protein synthesis inhibitor, on FMRFamide-induced depression.
Main Results:
- Five applications of FMRFamide over 2 hours induced long-term synaptic depression lasting 24 hours.
- FMRFamide-induced LTD was transmitter-specific; dopamine and low-frequency stimulation did not induce LTD.
- Long-term depression, unlike short-term depression, was blocked by anisomycin, indicating a requirement for protein synthesis.
Conclusions:
- Long-term synaptic depression in Aplysia, similar to long-term facilitation, requires protein synthesis.
- Heterosynaptic depression, like facilitation, exists in both short-term and long-term forms, with the latter dependent on gene products.
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