Journal Article

DZNE-2020-02498

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Ryanodine receptor-2 upregulation and nicotine-mediated plasticity.

Ziviani, E. ; Lippi, G. ; Bano, D. ; Munarriz, E. ; Guiducci, S. ; Zoli, M. ; Young, K. W. ; Nicotera, P. (Last author)DZNE*

2011
Wiley Hoboken, NJ [u.a.]

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Please use a persistent id in citations: doi:10.1038/emboj.2010.279

Abstract: Nicotine, the major psychoactive component of cigarette smoke, modulates neuronal activity to produce Ca2+-dependent changes in gene transcription. However, the downstream targets that underlie the long-term effects of nicotine on neuronal function, and hence behaviour, remain to be elucidated. Here, we demonstrate that nicotine administration to mice upregulates levels of the type 2 ryanodine receptor (RyR2), a Ca2+-release channel present on the endoplasmic reticulum, in a number of brain areas associated with cognition and addiction, notably the cortex and ventral midbrain. Nicotine-mediated RyR2 upregulation was driven by CREB, and caused a long-lasting reinforcement of Ca2+ signalling via the process of Ca2+-induced Ca2+ release. RyR2 upregulation was itself required for long-term phosphorylation of CREB in a positive-feedback signalling loop. We further demonstrate that inhibition of RyR-activation in vivo abolishes sensitization to nicotine-induced habituated locomotion, a well-characterised model for onset of drug dependence. Our findings, therefore, indicate that gene-dependent reprogramming of Ca2+ signalling is involved in nicotine-induced behavioural changes.

Keyword(s): Animals (MeSH) ; Calcium: metabolism (MeSH) ; Calcium Signaling: drug effects (MeSH) ; Cells, Cultured (MeSH) ; Cerebellar Cortex: cytology (MeSH) ; Cerebellar Cortex: drug effects (MeSH) ; Cyclic AMP Response Element-Binding Protein: metabolism (MeSH) ; Ganglionic Stimulants: administration & dosage (MeSH) ; Ganglionic Stimulants: pharmacology (MeSH) ; Male (MeSH) ; Mice (MeSH) ; Mice, Inbred C57BL (MeSH) ; Motor Activity: drug effects (MeSH) ; Nerve Net: drug effects (MeSH) ; Nerve Net: metabolism (MeSH) ; Neuronal Plasticity: drug effects (MeSH) ; Neurons: drug effects (MeSH) ; Neurons: metabolism (MeSH) ; Nicotine: administration & dosage (MeSH) ; Nicotine: pharmacology (MeSH) ; Rats (MeSH) ; Rats, Sprague-Dawley (MeSH) ; Ryanodine Receptor Calcium Release Channel: genetics (MeSH) ; Ryanodine Receptor Calcium Release Channel: metabolism (MeSH) ; Up-Regulation: drug effects (MeSH) ; Cyclic AMP Response Element-Binding Protein ; Ganglionic Stimulants ; Ryanodine Receptor Calcium Release Channel ; Nicotine ; Calcium

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Contributing Institute(s):

1. Aging and Neurodegeneration (AG Bano)
2. Synaptic Connectivity and Neurodegeneration (AG Nicotera)

Research Program(s):

1. 341 - Molecular Signaling (POF3-341) (POF3-341)
2. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)

Appears in the scientific report 2011

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Database coverage:
; BIOSIS Previews ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; Ebsco Academic Search ; IF >= 10 ; JCR ; NCBI Molecular Biology Database ; PubMed Central ; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Web of Science Core Collection

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