ArticleLearning & memory (Cold Spring Harbor, N.Y.)
TGF-beta1 in Aplysia: role in long-term changes in the excitability of sensory neurons and distribution of TbetaR-II-like immunoreactivity.
Article in Learning & memory (Cold Spring Harbor, N.Y.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 63 citations in OpenAlex.
- Recent advances in research on common targets of neurological and sex hormonal influences on asthma.Clinical and translational allergy · 2025Review
- Dynamics and Mechanisms of ERK Activation after Different Protocols that Induce Long-Term Synaptic Facilitation inOxford open neuroscience · 2023Article
- Defective synaptic plasticity in a model of Coffin-Lowry syndrome is rescued by simultaneously targeting PKA and MAPK pathways.Learning & memory (Cold Spring Harbor, N.Y.) · 2022Article
- Quantitative description of the interactions among kinase cascades underlying long-term plasticity of Aplysia sensory neurons.Scientific reports · 2021Article
- Role of p90 ribosomal S6 kinase in long-term synaptic facilitation and enhanced neuronal excitability.Scientific reports · 2020Article
- TGF-β/Smad3 Signalling Modulates GABA Neurotransmission: Implications in Parkinson's Disease.International journal of molecular sciences · 2020Review
- Astrocytes and the TGF-β1 Pathway in the Healthy and Diseased Brain: a Double-Edged Sword.Molecular neurobiology · 2019Review
- TGF-β Family Signaling in Neural and Neuronal Differentiation, Development, and Function.Cold Spring Harbor perspectives in biology · 2017Review
- A novel in vitro analog expressing learning-induced cellular correlates in distinct neural circuits.Learning & memory (Cold Spring Harbor, N.Y.) · 2017Article
- Superior long-term synaptic memory induced by combining dual pharmacological activation of PKA and ERK with an enhanced training protocol.Learning & memory (Cold Spring Harbor, N.Y.) · 2017Article
- The membrane trafficking and functionality of the K+-Cl- co-transporter KCC2 is regulated by TGF-β2.Journal of cell science · 2016Article
- Transforming growth factor β recruits persistent MAPK signaling to regulate long-term memory consolidation in Aplysia californica.Learning & memory (Cold Spring Harbor, N.Y.) · 2016Article
- The Contribution of Spatial and Temporal Molecular Networks in the Induction of Long-term Memory and Its Underlying Synaptic Plasticity.AIMS neuroscience · 2016Article
- A key role for TGF-β1 in hippocampal synaptic plasticity and memory.Scientific reports · 2015Article
- Aging in Sensory and Motor Neurons Results in Learning Failure in Aplysia californica.PloS one · 2015Article
- Doxorubicin attenuates serotonin-induced long-term synaptic facilitation by phosphorylation of p38 mitogen-activated protein kinase.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Behavioral aging is associated with reduced sensory neuron excitability in Aplysia californica.Frontiers in aging neuroscience · 2014Article
- TGFβ1 treatment reduces hippocampal damage, spontaneous recurrent seizures, and learning memory deficits in pilocarpine-treated rats.Journal of molecular neuroscience : MN · 2013Article
- Transforming growth factor beta induces sensory neuronal hyperexcitability, and contributes to pancreatic pain and hyperalgesia in rats with chronic pancreatitis.Molecular pain · 2012Article
- Increased transforming growth factor-β1 modulates glutamate receptor expression in the hippocampus.International journal of physiology, pathophysiology and pharmacology · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Exogenous recombinant human transforming growth factor beta-1 (TGF-beta1) induced long-term facilitation of Aplysia sensory-motor synapses. In addition, 5-HT-induced facilitation was blocked by application of a soluble fragment of the extracellular portion of the TGF-beta1 type II receptor (TbetaR-II), which presumably acted by scavenging an endogenous TGF-beta1-like molecule. Because TbetaR-II is essential for transmembrane signaling by TGF-beta, we sought to determine whether Aplysia tissues contained TbetaR-II and specifically, whether neurons expressed the receptor. Western blot analysis of Aplysia tissue extracts demonstrated the presence of a TbetaR-II-immunoreactive protein in several tissue types. The expression and distribution of TbetaR-II-immunoreactive proteins in the central nervous system was examined by immunohistochemistry to elucidate sites that may be responsive to TGF-beta1 and thus may play a role in synaptic plasticity. Sensory neurons in the ventral-caudal cluster of the pleural ganglion were immunoreactive for TbetaR-II, as well as many neurons in the pedal, abdominal, buccal, and cerebral ganglia. Sensory neurons cultured in isolation and cocultured sensory and motor neurons were also immunoreactive. TGF-beta1 affected the biophysical properties of cultured sensory neurons, inducing an increase of excitability that persisted for at least 48 hr. Furthermore, exposure to TGF-beta1 resulted in a reduction in the firing threshold of sensory neurons. These results provide further support for the hypothesis that TGF-beta1 plays a role in long-term synaptic plasticity in Aplysia.
Indexed as
Identifiers
10492013PMC311291W1947961740What 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.