ArticleBehavioural pharmacology2016
Neuronal calcium/calmodulin-dependent protein kinase II mediates nicotine reward in the conditioned place preference test in mice.
Article in Behavioural pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Dopamine D2 Receptors, D1/D2 Receptor Heteromers and CaMKII Signaling in the Neurobiology of Drug Addiction.Molecular neurobiology · 2026Review
- Nicotine combined with estrogen activates protein kinase PKCι and TAO, while inhibiting specific MAP kinase pathways in cultured human neurons: an atlas of kinase activities for nicotine use disorder.Frontiers in cellular neuroscience · 2026Article
- Synaptic Plasticity Linked to Ionotropic Glutamate Receptors After Nicotine Exposure.Current neuropharmacology · 2025Review
- Amelioration of Nicotine-Induced Conditioned Place Preference Behaviors in Mice by an FABP3 Inhibitor.International journal of molecular sciences · 2023Article
- Impaired Acquisition of Nicotine-Induced Conditioned Place Preference in Fatty Acid-Binding Protein 3 Null Mice.Molecular neurobiology · 2021Article
- The Role of CaMKII and ERK Signaling in Addiction.International journal of molecular sciences · 2021Review
- Effects of nicotine on DARPP-32 and CaMKII signaling relevant to addiction.Advances in pharmacology (San Diego, Calif.) · 2021Review
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Several recent studies have indicated the involvement of calcium-dependent mechanisms, in particular the abundant calcium-activated kinase, calcium/calmodulin-dependent kinase II (CaMKII), in behaviors associated with nicotine dependence in mice. Behavioral and biochemical studies have shown that CaMKII is involved in acute and chronic nicotine behaviors and nicotine withdrawal; however, evidence of a role for CaMKII in nicotine reward is lacking. Thus, the goal of the current study was to examine the role of CaMKII in nicotine reward. Using pharmacological and genetic tools, we tested nicotine conditioned place preference (CPP) in C57Bl/6 mice after administration of CaMKII antagonists and in α-CaMKII wild-type (+/+) and heterozygote (±) mice. CaMKII antagonists blocked expression of nicotine CPP, and the preference score was significantly reduced in α-CaMKII ± mice compared with their +/+ counterparts. Further, we assessed CaMKII activity in the ventral tegmental area (VTA), nucleus accumbens (NAc), prefrontal cortex, and hippocampus after nicotine CPP and found significant increases in CaMKII activity in the mouse VTA and NAc that were blocked by CaMKII antagonists. The findings from this study show that CaMKII mediates nicotine reward and suggest that increases in CaMKII activity in the VTA and NAc are relevant to nicotine reward behaviors.
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