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Learning and nicotine interact to increase CREB phosphorylation at the jnk1 promoter in the hippocampus

Learning and nicotine interact to increase CREB phosphorylation at the jnk1 promoter in the hippocampus
Learning and nicotine interact to increase CREB phosphorylation at the jnk1 promoter in the hippocampus
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 ?2-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 ?2-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.
1932-6203
e39939-[9pp]
Kenney, Justin W.
a498bbd6-750d-4778-bd72-6ea336c883e8
Poole, Rachel L.
cbd38b8a-5bbb-4c8e-b2e5-a4283200f165
Adoff, Michael D.
ddb2e65a-2a75-4541-8b6f-45894b11ca62
Logue, Sheree F.
85fe2c3e-125e-44ed-ab6f-6bb8a0c1d960
Gould, Thomas J.
de84ac91-2b6f-4524-b4d3-1f210047c57a
Kenney, Justin W.
a498bbd6-750d-4778-bd72-6ea336c883e8
Poole, Rachel L.
cbd38b8a-5bbb-4c8e-b2e5-a4283200f165
Adoff, Michael D.
ddb2e65a-2a75-4541-8b6f-45894b11ca62
Logue, Sheree F.
85fe2c3e-125e-44ed-ab6f-6bb8a0c1d960
Gould, Thomas J.
de84ac91-2b6f-4524-b4d3-1f210047c57a

Kenney, Justin W., Poole, Rachel L., Adoff, Michael D., Logue, Sheree F. and Gould, Thomas J. (2012) Learning and nicotine interact to increase CREB phosphorylation at the jnk1 promoter in the hippocampus. PLoS ONE, 7 (6), e39939-[9pp]. (doi:10.1371/journal.pone.0039939). (PMID:22761932)

Record type: Article

Abstract

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 ?2-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 ?2-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.

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Published date: 28 June 2012
Organisations: Molecular and Cellular

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Local EPrints ID: 343515
URI: http://eprints.soton.ac.uk/id/eprint/343515
ISSN: 1932-6203
PURE UUID: 30ca12e9-a5d6-4b89-84a2-a2425afc48d7

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Date deposited: 08 Oct 2012 11:44
Last modified: 14 Mar 2024 12:04

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Contributors

Author: Justin W. Kenney
Author: Rachel L. Poole
Author: Michael D. Adoff
Author: Sheree F. Logue
Author: Thomas J. Gould

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