Learning and nicotine interact to increase CREB phosphorylation at the jnk1 promoter in the hippocampus
| Autor: | Sheree F. Logue, Rachel L. Poole, Justin W. Kenney, Thomas J. Gould, Michael D. Adoff |
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| Jazyk: | angličtina |
| Rok vydání: | 2012 |
| Předmět: |
Mouse
Psychopharmacology lcsh:Medicine Hippocampus Polymerase Chain Reaction Nicotine Behavioral Neuroscience 0302 clinical medicine Learning and Memory Molecular Cell Biology Membrane Receptor Signaling Fear conditioning Phosphorylation Cyclic AMP Response Element-Binding Protein Promoter Regions Genetic lcsh:Science 0303 health sciences Multidisciplinary Neurotransmitter Receptor Signaling Fear Animal Models Cell biology Nicotinic agonist Behavioral Pharmacology Medicine Electrophoresis Polyacrylamide Gel medicine.drug Research Article Signal Transduction Chromatin Immunoprecipitation Drugs and Devices Biology CREB Signaling Pathways 03 medical and health sciences Histone H3 Model Organisms Neuropharmacology medicine Learning Mitogen-Activated Protein Kinase 8 Transcription factor 030304 developmental biology DNA Primers Base Sequence lcsh:R Promoter Molecular biology biology.protein lcsh:Q Molecular Neuroscience Chromatin immunoprecipitation 030217 neurology & neurosurgery Neuroscience |
| Zdroj: | PLoS ONE, Vol 7, Iss 6, p e39939 (2012) PLoS ONE |
| ISSN: | 1932-6203 |
| Popis: | Nicotine is known to enhance long-term hippocampus dependent learning and memory in both rodents and humans via its activity at nicotinic acetylcholinergic receptors (nAChRs). However, the molecular basis for the nicotinic modulation of learning is incompletely understood. Both the mitogen activated protein kinases (MAPKs) and cAMP response element binding protein (CREB) are known to be integral to the consolidation of long-term memory and the disruption of MAPKs and CREB are known to abrogate some of the cognitive effects of nicotine. In addition, the acquisition of contextual fear conditioning in the presence of nicotine is associated with a β2-subunit containing nAChR-dependent increase in jnk1 (mapk8) transcription in the hippocampus. In the present study, chromatin immunoprecipitation (ChIP) was used to examine whether learning and nicotine interact to alter transcription factor binding or histone acetylation at the jnk1 promoter region. The acquisition of contextual fear conditioning in the presence of nicotine resulted in an increase in phosphorylated CREB (pCREB) binding to the jnk1 promoter in the hippocampus in a β2-subunit containing nAChR dependent manner, but had no effect on CREB binding; neither fear conditioning alone nor nicotine administration alone altered transcription factor binding to the jnk1 promoter. In addition, there were no changes in histone H3 or H4 acetylation at the jnk1 promoter following fear conditioning in the presence of nicotine. These results suggest that contextual fear learning and nicotine administration act synergistically to produce a unique pattern of protein activation and gene transcription in the hippocampus that is not individually generated by fear conditioning or nicotine administration alone. |
| Databáze: | OpenAIRE |
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