Abstract
Nicotine is the predominant addictive compound of tobacco and causes the acquisition of dependence through its interactions with nicotinic acetylcholine receptors and various neurotransmitter releases in the central nervous system. The Ca2+/calmodulin-dependent protein kinase II (CaMKII) and extracellular signal-regulated kinase (ERK) play a pivotal role in synaptic plasticity in the hippocampus. CaMKII is involved in long-term potentiation induction, which underlies the consolidation of learning and memory; however, the roles of CaMKII in nicotine and other psychostimulant-induced addiction still require further investigation. This article reviews the molecular mechanisms and crucial roles of CaMKII and ERK in nicotine and other stimulant drug-induced addiction. We also discuss dopamine (DA) receptor signaling involved in nicotine-induced addiction in the brain reward circuitry. In the last section, we introduce the association of polyunsaturated fatty acids and cellular chaperones of fatty acid-binding protein 3 in the context of nicotine-induced addiction in the mouse nucleus accumbens and provide a novel target for the treatment of drug abuse affecting dopaminergic systems.
Highlights
Smoking was the second leading cause of early death and disability in 2015 [1]
We focus on the mechanisms of calmodulin-dependent protein kinase II (CaMKII) and extracellular signal-regulated kinase (ERK), which is mediated by CaMKII function in the brain reward system, in the context of nicotine and other psychostimulant-induced addiction
The mesolimbic DAergic projections originating from the ventral tegmental area (VTA) and projected to the nucleus accumbens (NAc) and the prefrontal cortex (PFC) are susceptible to electrical stimulation
Summary
Smoking was the second leading cause of early death and disability in 2015 [1]. People are inclined to use tobacco continually despite the harmful consequences. Other psychostimulant drugs, such as morphine, cocaine, and amphetamine, are similar to nicotine: they participate and modulate the brain reward system and motivation though they have different interaction sites and chemical structures [10]. We consider the participation of CaMKII in both dopamine D1 receptor (D1R) and dopamine D2 receptor (D2R) signaling, provide fatty acid-binding protein 3 (FABP3) as a novel target, and clarify the underlying mechanisms in terms of nicotine and other psychostimulant-induced addiction affecting the dopaminergic (DAergic) system
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