Cited by 118Neuroscience and Neuropharmacology ResearchMemory and Neural MechanismsNeurobiology and Insect Physiology Research

Reversal of synaptic depression by serotonin at Aplysia sensory neuron synapses involves activation of adenylyl cyclase.

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Goldsmith, B A, Abrams, T W·1991·Proceedings of the National Academy of Sciences

Abstract

Facilitation of the monosynaptic connection between siphon sensory neurons and gill and siphon motor neuron contributes to sensitization and dishabituation of the gill and siphon withdrawal reflex in Aplysia. The facilitatory transmitter serotonin (5-HT) initiates two mechanisms that act in parallel to increase transmitter release from siphon sensory neurons. 5-HT acts, at least partly through cAMP, to broaden the presynaptic action potential. 5-HT also initiates a second process that facilitates depressed sensory neuron synapses by a mechanism independent of changes in action potential duration. Recent experiments indicated that either of two protein kinases, cAMP-dependent protein kinase A and protein kinase C, are capable of effectively activating this second facilitatory mechanism, restoring synaptic transmission in depressed synapses. We have used the adenylyl cyclase inhibitor SQ 22,536 [9-(tetrahydro-2-furyl)adenine or THFA] to explore the contribution of cAMP to the reversal of synaptic depression. THFA effectively inhibited both adenylyl cyclase activity in vitro and known cyclase-mediated effects in intact sensory neurons. THFA also completely blocked facilitation of depressed synapses by 5-HT. These results suggest that adenylyl cyclase plays a critical role in the reversal of synaptic depression that contributes to dishabituation in this system.

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Crossref · 10.1073/pnas.88.20.9021

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Authors
Goldsmith, B. A., & Abrams, T. W.
Affiliations
University of Pennsylvania (US)
Venue
Proceedings of the National Academy of Sciences
Published
1991-10-15
Volume
88
Issue
20
Pages
9021-9025
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2054343388
Cited by
118
References
38
Citations by year
2024: 1 · 2023: 1 · 2016: 1 · 2014: 1
FWCI
1.83
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Whitehall Foundation
  • National Institutes of Health (5r01ns025788-05)
  • National Institute of Neurological Disorders and Stroke (NS 25788)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurobiology and Insect Physiology Research
Keywords
synaptic depression, serotonin, adenylate cyclase, Aplysia, cyclic AMP, dishabituation, presynaptic action potential, protein kinase C, protein kinase A, synaptic transmission
MeSH terms
Adenylyl Cyclase Inhibitors, Adenine, Adenylyl Cyclases, Animals, Aplysia, Enzyme Activation, Evoked Potentials, Ganglia, Kinetics, Neurons, Afferent, Serotonin, Synapses, Phorbol 12,13-Dibutyrate, In Vitro Techniques

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