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Transient versus persistent functional and structural changes associated with facilitation of Aplysia sensorimotor
1Center for Neurobiology and Behavior, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA.
Summary
Serotonin (5-HT) enhances Aplysia sensorimotor synapses via protein kinase A (PKA) and protein kinase C (PKC). PKA and PKC mediate short-term synaptic changes, while PKA also sustains long-term facilitation.
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Background:
- Serotonin (5-HT) is known to modulate synaptic plasticity.
- Protein kinase A (PKA) and protein kinase C (PKC) are key signaling molecules involved in cellular processes.
Purpose of the Study:
- To investigate the roles of PKA and PKC in short-term and long-term facilitation of Aplysia sensorimotor synapses.
- To elucidate the mechanisms underlying serotonin-evoked synaptic plasticity.
Main Methods:
- Manipulating cAMP levels in sensory neurons.
- Treating sensory neurons with phorbol esters to activate PKC.
- Assessing synaptic efficacy and the number of sensory neuron varicosities.
- Observing neurite extension and growth cone behavior.
Main Results:
- Increased cAMP levels led to persistent increases in synaptic efficacy and varicosity number.
- Phorbol ester treatment caused transient increases in synaptic efficacy and varicosity number.
- PKC activation by phorbol esters reduced neurite extension and caused growth cone retraction, which were reversible.
Conclusions:
- Both PKA and PKC contribute to short- and intermediate-term synaptic facilitation.
- PKA activity is crucial for the long-term maintenance of synaptic facilitation.
- Serotonin-induced synaptic plasticity involves complex regulation of both synaptic efficacy and neuronal structure.