Abstract：
:Short-term augmentation of synaptic transmission at sensory neuron synapses of Aplysia contributes to behavioral sensitization and is one of the current models for a cellular mechanism of learning. This neuromodulatory process, mediated at least in part by the facilitatory neurotransmitter serotonin (5-HT) acting through cAMP, has been thought to result largely from prolongation of the sensory neuron action potential (AP). The quantitative contribution of AP prolongation to synaptic augmentation was examined using a new culture preparation that is favorable for controlling the voltage at the presynaptic terminals. Preventing AP prolongation by using unvarying voltage-clamp commands in place of triggered APs did not reduce augmentation significantly, and pharmacological prolongation of APs caused by a high concentration of 5-HT led to a negligible increase in the synaptic response. Together with earlier evidence against the involvement of changes in Ca2+ current, these results suggest that synaptic augmentation may result from modulation of steps in the secretory process that lie distal to the flow of ion currents across the nerve terminal membrane.
journal_name
Neuronjournal_title
Neuronauthors
Klein Mdoi
10.1016/0896-6273(94)90466-9subject
Has Abstractpub_date
1994-07-01 00:00:00pages
159-66issue
1eissn
0896-6273issn
1097-4199pii
0896-6273(94)90466-9journal_volume
13pub_type
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