The cellular and molecular details of the synaptic connections
are shown in Figure 19.4. The sensory signal registering the aversive
stimulus to the tail leads to the release of serotonin that activates
serotonin receptors located on the axon terminals of sensory neurons
from the siphon. Serotonin activates G-protein-coupled serotonin
receptors, initiating the following sequence of events: activated G-
protein > activated adenylate cyclase > increased cAMP synthesis
activated cAMP-dependent protein kinase A (PKA) > phosphory-
lated potassium-leak channels located in the membrane of the axon
terminal > closed potassium-leak channels > decreased outward
K* current ~ prolonged depolarizing phase of action potential >
voltage-gated Ca channels opened longer > greater Ca influx into
axon terminal ~ increased release of glutamate neurotransmitter
increased excitation of postsynaptic motor neuron mediating gill
retraction.
Following a single aversive stimulus to the tail, the increased
robustness of the gill-withdrawal response lasts about an hour—a
kind of short-term memory. As with many types of memory, repeti-
tion results in strengthening. In this case, if the aversive stimulus to
the tail is repeated several times, then the increased robustness of gill
withdrawal in response to touching the siphon may be maintained
for many days—a kind of long-term memory. Here’s how: the repeated
activation of serotonin receptors results in higher intracellular levels
of cAMP, leading to more sustained activation of PKA (per the scenario
described above). Some of the activated PKA now makes its way to the
cell nucleus, where it catalyzes the phosphorylation of transcription
factor proteins, resulting in the transcription of particular genes. One
of these genes codes for ubiquitin hydrolase, which helps cleave off
a regulatory subunit of PKA, resulting in the PKA remaining in an
activated state even in the absence of cAMP. This produces a persis-