Nicotinic regulation of CREB activation in hippocampal neurons by glutamatergic and nonglutamatergic pathways. Mol Cell Neurosci 2002 Dec;21(4):616-25
Date
12/31/2002Pubmed ID
12504594DOI
10.1006/mcne.2002.1202Scopus ID
2-s2.0-0036941840 (requires institutional sign-in at Scopus site) 105 CitationsAbstract
Activity-dependent gene expression is essential for form and function in the nervous system. Best understood is the role of glutamatergic signaling in controlling such events, but nicotinic signaling can also regulate transcription. We show here that nicotine can alter gene expression in rat hippocampal neurons, as reflected by activation of the transcription factor CREB and appearance of the immediate early gene product c-Fos. The process depends on both CaM and MAP kinases and on calcium release from internal stores. Part of the nicotinic effect is mediated via glutamatergic transmission, even in the absence of action potentials. Voltage-gated calcium channels are not necessary for nicotine-induced activation of CREB in hippocampal neurons. The low levels of sustained nicotinic stimulation required for transcriptional effects are consistent with those likely to be achievable either by the normal septal cholinergic innervation of the hippocampus or by repeated tobacco usage.
Author List
Hu M, Liu QS, Chang KT, Berg DKAuthor
Qing-song Liu PhD Professor in the Pharmacology and Toxicology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AcetylcholineAnimals
Calcium Channels
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Calcium-Calmodulin-Dependent Protein Kinases
Cell Nucleus
Cells, Cultured
Cyclic AMP Response Element-Binding Protein
Gene Expression Regulation, Developmental
Glutamic Acid
Hippocampus
Neural Pathways
Neuronal Plasticity
Neurons
Nicotine
Proto-Oncogene Proteins c-fos
Rats
Rats, Sprague-Dawley
Receptors, Nicotinic
Synapses
Synaptic Transmission
alpha7 Nicotinic Acetylcholine Receptor
