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Long-term facilitation in Aplysia involves increase in transmitter release.
N Dale1, S Schacher, E R Kandel
1Howard Hughes Medical Institute, College of Physicians and Surgeons of Columbia University, New York State Psychiatric Institute, NY 10032.
Science (New York, N.Y.)
|January 15, 1988
Summary
Long-term memory enhancement in Aplysia involves increased synaptic transmission. This study shows that repeated 5-hydroxytryptamine applications enhance memory by increasing the number of transmitter quanta released, not postsynaptic receptor sensitivity.
Area of Science:
- Neuroscience
- Cellular Biology
- Molecular Biology
Background:
- Long-lasting synaptic enhancement is crucial for memory storage in many species.
- The precise mechanism, whether increased transmitter release or postsynaptic receptor sensitivity, remains unclear.
Purpose of the Study:
- To investigate the cellular mechanisms underlying long-term synaptic facilitation in Aplysia.
- To determine if facilitation results from enhanced neurotransmitter release or increased postsynaptic receptor sensitivity.
Main Methods:
- Utilized microcultures of single sensory and motor neurons from Aplysia.
- Performed quantal analysis of miniature excitatory postsynaptic potentials (mEPSPs).
- Analyzed long-term facilitation induced by 5-hydroxytryptamine (5-HT).
Main Results:
- Quantal analysis revealed that 5-HT induced long-term facilitation.
- The facilitation was attributed to an increase in the number of transmitter quanta released.
- No significant change in postsynaptic receptor sensitivity was observed.
Conclusions:
- Long-term synaptic facilitation in Aplysia is mediated by an increase in presynaptic transmitter release.
- This finding clarifies the mechanism of memory storage at the synaptic level.