ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Doxorubicin attenuates serotonin-induced long-term synaptic facilitation by phosphorylation of p38 mitogen-activated protein kinase.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 39 citations in OpenAlex.
- Chemobrain as a Neuroimmune Syndrome: Mechanisms, Modifiers, and Emerging Multi-Target Therapeutic Strategies.Molecules (Basel, Switzerland) · 2026Review
- The Right Time for a Synapse to Change: Windows and Mechanisms of Multiday Training Trials.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Long-term dynamic profiles of cognitive kinases induced by different learning protocols.bioRxiv : the preprint server for biology · 2025Article
- Doxorubicin treatment has a biphasic effect over time on dopamine release and impulsive behavior in Wistar rats.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- The challenge of chemotherapy-related cognitive impairment: assessing and managing cognitive decline after cancer treatment.Ecancermedicalscience · 2025Review
- Neurotoxicity of the antineoplastic drugs: "Doxorubicin" as an example.Journal of molecular histology · 2024Review
- 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
- Activation of SIRT-1 Pathway by Nanoceria Sheds Light on Its Ameliorative Effect on Doxorubicin-Induced Cognitive Impairment (Chemobrain): Restraining Its Neuroinflammation, Synaptic Dysplasticity and Apoptosis.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Cognitive adverse effects of chemotherapy and immunotherapy: are interventions within reach?Nature reviews. Neurology · 2022Review
- Chemotherapy-induced cognitive impairment: focus on the intersection of oxidative stress and TNFα.Cellular and molecular life sciences : CMLS · 2021Review
- Doxorubicin-Induced Cognitive Impairment: The Mechanistic Insights.Frontiers in oncology · 2021Review
- Postsynaptic effects ofLearning & memory (Cold Spring Harbor, N.Y.) · 2020Article
- Chemotherapy-Induced Cognitive Impairment Is Associated with Increased Inflammation and Oxidative Damage in the Hippocampus.Molecular neurobiology · 2019Article
- Plausible biochemical mechanisms of chemotherapy-induced cognitive impairment ("chemobrain"), a condition that significantly impairs the quality of life of many cancer survivors.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- Peroxisomes contribute to oxidative stress in neurons during doxorubicin-based chemotherapy.Molecular and cellular neurosciences · 2018Article
- Article
- Characterization and reversal of Doxorubicin-mediated biphasic activation of ERK and persistent excitability in sensory neurons of Aplysia californica.Scientific reports · 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
- Neurovascular Interaction Promotes the Morphological and Functional Maturation of Cortical Neurons.Frontiers in cellular neuroscience · 2017Article
- Naringin and Sertraline Ameliorate Doxorubicin-Induced Behavioral Deficits Through Modulation of Serotonin Level and Mitochondrial Complexes Protection Pathway in Rat Hippocampus.Neurochemical research · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Doxorubicin (DOX) is an anthracycline used widely for cancer chemotherapy. Its primary mode of action appears to be topoisomerase II inhibition, DNA cleavage, and free radical generation. However, in non-neuronal cells, DOX also inhibits the expression of dual-specificity phosphatases (also referred to as MAPK phosphatases) and thereby inhibits the dephosphorylation of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (p38 MAPK), two MAPK isoforms important for long-term memory (LTM) formation. Activation of these kinases by DOX in neurons, if present, could have secondary effects on cognitive functions, such as learning and memory. The present study used cultures of rat cortical neurons and sensory neurons (SNs) of Aplysia to examine the effects of DOX on levels of phosphorylated ERK (pERK) and phosphorylated p38 (p-p38) MAPK. In addition, Aplysia neurons were used to examine the effects of DOX on long-term enhanced excitability, long-term synaptic facilitation (LTF), and long-term synaptic depression (LTD). DOX treatment led to elevated levels of pERK and p-p38 MAPK in SNs and cortical neurons. In addition, it increased phosphorylation of the downstream transcriptional repressor cAMP response element-binding protein 2 in SNs. DOX treatment blocked serotonin-induced LTF and enhanced LTD induced by the neuropeptide Phe-Met-Arg-Phe-NH2. The block of LTF appeared to be attributable to overriding inhibitory effects of p-p38 MAPK, because LTF was rescued in the presence of an inhibitor (SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)-1H-imidazole]) of p38 MAPK. These results suggest that acute application of DOX might impair the formation of LTM via the p38 MAPK pathway.
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