ReviewBrain research2012
Two independent forms of activity-dependent potentiation regulate electrical transmission at mixed synapses on the Mauthner cell.
Review in Brain research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Identification of Dopaminergic Neurons That Can Both Establish Associative Memory and Acutely Terminate Its Behavioral Expression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Electrical synapses regulate both subthreshold integration and population activity of principal cells in response to transient inputs within canonical feedforward circuits.PLoS computational biology · 2019Article
- Article
- Gap junction plasticity as a mechanism to regulate network-wide oscillations.PLoS computational biology · 2018Article
- A calcium-dependent pathway underlies activity-dependent plasticity of electrical synapses in the thalamic reticular nucleus.The Journal of physiology · 2017Article
- Structural and Functional Consequences of Connexin 36 (Cx36) Interaction with Calmodulin.Frontiers in molecular neuroscience · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Mixed (electrical and chemical) synaptic contacts on the Mauthner cells, known as Club endings, constitute a valuable model for the study of vertebrate electrical transmission. While electrical synapses are still perceived by many as passive intercellular channels that lack modifiability, a wealth of experimental evidence shows that gap junctions at Club endings are subject to dynamic regulatory control by two independent activity-dependent mechanisms that lead to potentiation of electrical transmission. One of those mechanisms relies on activation of NMDA receptors and postsynaptic CaMKII. A second mechanism relies on mGluR activation and endocannabinoid production and is indirectly mediated via the release of dopamine from nearby varicosities, which in turn leads to potentiation of the synaptic response via a PKA-mediated postsynaptic mechanism. We review here these two forms of potentiation and their signaling mechanisms, which include the activation of two kinases with well-established roles as regulators of synaptic strength, as well as the functional implications of these two forms of potentiation. Special Issue entitled Electrical Synapses.
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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.