Abstract
The cAMP pathway plays a critical role in synaptic plasticity. We assessed using the ectopic expression of octopamine (OA) receptor, the contribution of the cAMP pathway to short-term facilitation of sensory–motor synapses in Aplysia. When synaptic connections were depressed to 20–30% of their initial EPSP amplitude, the application of OA to sensory cells expressing OA receptor showed significant synaptic facilitation, but this was less than the synaptic facilitation shown by 5-HT treatment. We also found that synaptic facilitation was further enhanced when OA was treated in the presence of 5-HT at non-depressed synapses, but not at depressed synapses. These results imply that the role of cAMP in synaptic facilitation is reduced as the synapse becomes depressed due to repeated activity.
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