ArticleMolecular and cellular neurosciences2009
Direct enhancement of presynaptic calcium influx in presynaptic facilitation at Aplysia sensorimotor synapses.
Article in Molecular and cellular neurosciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- The role of specific isoforms of CaScientific reports · 2023Article
- The CaScientific reports · 2018Article
- Contribution of PKC to the maintenance of 5-HT-induced short-term facilitation at sensorimotor synapses of Aplysia.Journal of neurophysiology · 2014Article
- Peptide-induced modulation of synaptic transmission and escape response in Drosophila requires two G-protein-coupled receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Presynaptic and postsynaptic mechanisms of synaptic plasticity and metaplasticity during intermediate-term memory formation in Aplysia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Regulation of synaptic transmission by modulation of the calcium influx that triggers transmitter release underlies different forms of synaptic plasticity, and thus could contribute to learning. In the mollusk Aplysia, the neuromodulator serotonin (5-HT) increases evoked transmitter release from sensory neurons and thereby contributes to dishabituation and sensitization of defensive reflexes. We combined electrophysiological recording with fluorescence measurements of intracellular calcium in sensory neuron synapses in culture to test whether direct up-modulation by 5-HT of calcium influx triggered by single action potentials contributes to facilitation of transmitter release. We observe increases in a previously undescribed calcium influx that are strongly correlated with increases in the amplitude of the evoked postsynaptic potentials and which cannot be accounted for by action potential prolongation. Our results suggest that direct modulation of a presynaptic calcium conductance that controls neurotransmitter release contributes to the presynaptic facilitation that underlies a simple form of learning.
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Registered trials
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