ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Ca2+-independent protein kinase C Apl II mediates the serotonin-induced facilitation at depressed aplysia sensorimotor synapses.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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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.
The trial behind it
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Who cites it
40 citing papers in PubMed, 76 citations in OpenAlex.
- Article
- Selective Erasure of Distinct Forms of Long-Term Synaptic Plasticity Underlying Different Forms of Memory in the Same Postsynaptic Neuron.Current biology : CB · 2017Article
- Cell-Specific PKM Isoforms Contribute to the Maintenance of Different Forms of Persistent Long-Term Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Investigating the Potential Signaling Pathways That Regulate Activation of the Novel PKC Downstream of Serotonin in Aplysia.PloS one · 2016Article
- cJun and CREB2 in the postsynaptic neuron contribute to persistent long-term facilitation at a behaviorally relevant synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Decline in the Recovery from Synaptic Depression in Heavier Aplysia Results from Decreased Serotonin-Induced Novel PKC Activation.PloS one · 2015Article
- Contribution of PKC to the maintenance of 5-HT-induced short-term facilitation at sensorimotor synapses of Aplysia.Journal of neurophysiology · 2014Article
- Calcium-dependent PKC isoforms have specialized roles in short-term synaptic plasticity.Neuron · 2014Article
- Rescue of tau-induced synaptic transmission pathology by paclitaxel.Frontiers in cellular neuroscience · 2014Article
- Protein kinase C activation decreases peripheral actin network density and increases central nonmuscle myosin II contractility in neuronal growth cones.Molecular biology of the cell · 2013Article
- Release properties of individual presynaptic boutons expressed during homosynaptic depression and heterosynaptic facilitation of the Aplysia sensorimotor synapse.Frontiers in cellular neuroscience · 2013Article
- Serotonin-induced cleavage of the atypical protein kinase C Apl III in Aplysia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Protein kinase C acts as a molecular detector of firing patterns to mediate sensory gating in Aplysia.Nature neuroscience · 2012Article
- Massed training-induced intermediate-term operant memory in aplysia requires protein synthesis and multiple persistent kinase cascades.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- The rates of protein synthesis and degradation account for the differential response of neurons to spaced and massed training protocols.PLoS computational biology · 2011Article
- Persistent long-term synaptic plasticity requires activation of a new signaling pathway by additional stimuli.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Live-imaging of PKC translocation in Sf9 cells and in aplysia sensory neurons.Journal of visualized experiments : JoVE · 2011Article
- Whereas short-term facilitation is presynaptic, intermediate-term facilitation involves both presynaptic and postsynaptic protein kinases and protein synthesis.Learning & memory (Cold Spring Harbor, N.Y.) · 2011Article
- State-dependent disruption of short-term facilitation due to overexpression of the apPDE4 supershort form in Aplysia.Molecules and cells · 2011Article
- Aplysia cell adhesion molecule and a novel protein kinase C activity in the postsynaptic neuron are required for presynaptic growth and initial formation of specific synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
At nondepressed Aplysia sensory to motor synapses, serotonin (5-HT) facilitates transmitter release primarily through a protein kinase A pathway. In contrast, at depressed Aplysia sensory to motor synapses, 5-HT facilitates transmitter release primarily through a protein kinase C (PKC)-dependent pathway. It is known that only two phorbol ester-activated PKC isoforms, the Ca(2+)-dependent PKC Apl I and the Ca(2+)-independent PKC Apl II, exist in the Aplysia nervous system. For the first time, we have now been able to functionally determine which isoform of PKC is involved in a particular form of plasticity. We microinjected cultured sensorimotor pairs of neurons with various PKC constructs tagged with the enhanced green fluorescent protein as a reporter for successful plasmid expression. Our results demonstrate that short-term facilitation of depressed synapses is mediated by PKC Apl II. Dominant-negative PKC Apl II, but not dominant-negative PKC Apl I, disrupted the normal kinetics of 5-HT-induced facilitation by completely blocking its rapid onset. This effect was specific to depressed synapses, because dominant-negative PKC Apl II did not inhibit 5-HT-mediated facilitation of nondepressed synapses. Our results suggest that not only different signal transduction pathways but also different isoforms of a specific cascade may mediate physiological responses according to the state of a synapse.
Indexed as
Identifiers
11160395PMC6762221W2138595433What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.