The large size of the sea slug's nerve cells and its robust gill- and siphon-withdrawal reflex have enabled researchers to demonstrate that repeated exposure to serotonin, a modulatory neurotransmitter that plays a key part in learning in Aplysia, induces LTF at the sensorimotor synapse. It does so by increasing the expression and release of the neuropeptide sensorin from the pre-synaptic sensory neuron. It is thought that, by binding to autoreceptors, sensorin activates signal-transduction pathways involving mitogen-activated protein kinases (MAPKs) that lead to long-term changes in synaptic strength. However, the involvement of postsynaptic cellular events was unclear.
Using co-cultures of Aplysia pleural sensory neurons and small siphon-type motor neurons, Glanzman and colleagues show that LTF requires an increase in intracellular Ca2+ levels and protein synthesis in the postsynaptic neuron. Injection of a Ca2+ chelator into the postsynaptic neuron or treatment with membrane-impermeant protein-synthesis inhibitors prevented serotonin-induced LTF, as measured by changes in excitatory postsynaptic potential (EPSP) amplitude. Moreover, chelating intracellular Ca2+ in the postsynaptic neuron blocked the serotonin-induced increase in sensorin expression in the presynaptic sensory neuron. This finding raises the intriguing possibility that serotonin acts directly on the postsynaptic neuron, through the activation of G-protein-coupled receptors, to trigger not only an increase in Ca2+ but also the release of one or more retrograde signals that mediate the effect of serotonin on presynaptic sensorin expression.
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