ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Hippocampal c-Jun-N-terminal kinases serve as negative regulators of associative learning.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 63 citations in OpenAlex.
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- Role of Mitogen-Activated Protein (MAP) Kinase Pathways in Metabolic Diseases.Genome integrity · 2024Review
- Radiolabeled Aminopyrazoles as Novel Isoform Selective Probes for pJNK3 Quantification.ACS medicinal chemistry letters · 2022Article
- Enzymatic Degradation of Cortical Perineuronal Nets Reverses GABAergic Interneuron Maturation.Molecular neurobiology · 2022Article
- The schizophrenia risk gene Map2k7 regulates responding in a novel contingency-shifting rodent touchscreen gambling task.Disease models & mechanisms · 2022Article
- On the effect of hippocampal c-Jun N-terminal kinase inhibition on object recognition memory.Frontiers in behavioral neuroscience · 2022Article
- Causal roles of stress kinase JNK2 in DNA methylation and binge alcohol withdrawal-evoked behavioral deficits.Pharmacological research · 2021Article
- Photobiomodulation suppresses JNK3 by activation of ERK/MKP7 to attenuate AMPA receptor endocytosis in Alzheimer's disease.Aging cell · 2021Article
- Article
- Mimicking Age-Associated Gadd45γ Dysregulation Results in Memory Impairments in Young Adult Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Behavioral defects induced by chronic social defeat stress are protected byAnnals of translational medicine · 2019Article
- Neurochemical and molecular mechanisms underlying the retrieval-extinction effect.Psychopharmacology · 2019Review
- Kinase and Phosphatase Engagement Is Dissociated Between Memory Formation and Extinction.Frontiers in molecular neuroscience · 2019Article
- The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's Dementia.Frontiers in aging neuroscience · 2019Article
- Characterization of Behavioral, Signaling and Cytokine Alterations in a Rat Neurodevelopmental Model for Schizophrenia, and Their Reversal by the 5-HTMolecular neurobiology · 2018Article
- JIP1-Mediated JNK Activation Negatively Regulates Synaptic Plasticity and Spatial Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
In the adult mouse, signaling through c-Jun N-terminal kinases (JNKs) links exposure to acute stress to various physiological responses. Inflammatory cytokines, brain injury and ischemic insult, or exposure to psychological acute stressors induce activation of hippocampal JNKs. Here we report that exposure to acute stress caused activation of JNKs in the hippocampal CA1 and CA3 subfields, and impaired contextual fear conditioning. Conversely, intrahippocampal injection of JNKs inhibitors sp600125 (30 μm) or D-JNKI1 (8 μm) reduced activity of hippocampal JNKs and rescued stress-induced deficits in contextual fear. In addition, intrahippocampal administration of anisomycin (100 μg/μl), a potent JNKs activator, mimicked memory-impairing effects of stress on contextual fear. This anisomycin-induced amnesia was abolished after cotreatment with JNKs selective inhibitor sp600125 without affecting anisomycin's ability to effectively inhibit protein synthesis as measured by c-Fos immunoreactivity. We also demonstrated milder and transient activation of the JNKs pathway in the CA1 subfield of the hippocampus during contextual fear conditioning and an enhancement of contextual fear after pharmacological inhibition of JNKs under baseline conditions. Finally, using combined biochemical and transgenic approaches with mutant mice lacking different members of the JNK family (Jnk1, Jnk2, and Jnk3), we provided evidence that JNK2 and JNK3 are critically involved in stress-induced deficit of contextual fear, while JNK1 mainly regulates baseline learning in this behavioral task. Together, these results support the possibility that hippocampal JNKs serve as a critical molecular regulator in the formation of contextual fear.
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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.