TY - JOUR
T1 - Cellular, molecular, and genetic substrates underlying the impact of nicotine on learning
AU - Gould, Thomas J.
AU - Leach, Prescott T.
N1 - Funding Information:
Portions of the work reviewed here were supported by grants from the NIH: DA017949 (T.J.G.), DA024787 (T.J.G.), and CA143187 (Caryn Lerman). P.T.L. was supported by NIH training grant: DA007237. The authors would also like to acknowledge Sheree Logue and Tatiana Kazdoba for critical reading of this manuscript.
PY - 2014/1
Y1 - 2014/1
N2 - Addiction is a chronic disorder marked by long-lasting maladaptive changes in behavior and in reward system function. However, the factors that contribute to the behavioral and biological changes that occur with addiction are complex and go beyond reward. Addiction involves changes in cognitive control and the development of disruptive drug-stimuli associations that can drive behavior. A reason for the strong influence drugs of abuse can exert on cognition may be the striking overlap between the neurobiological substrates of addiction and of learning and memory, especially areas involved in declarative memory. Declarative memories are critically involved in the formation of autobiographical memories, and the ability of drugs of abuse to alter these memories could be particularly detrimental. A key structure in this memory system is the hippocampus, which is critically involved in binding multimodal stimuli together to form complex long-term memories. While all drugs of abuse can alter hippocampal function, this review focuses on nicotine. Addiction to tobacco products is insidious, with the majority of smokers wanting to quit; yet the majority of those that attempt to quit fail. Nicotine addiction is associated with the presence of drug-context and drug-cue associations that trigger drug seeking behavior and altered cognition during periods of abstinence, which contributes to relapse. This suggests that understanding the effects of nicotine on learning and memory will advance understanding and potentially facilitate treating nicotine addiction. The following sections examine: (1) how the effects of nicotine on hippocampus-dependent learning change as nicotine administration transitions from acute to chronic and then to withdrawal from chronic treatment and the potential impact of these changes on addiction, (2) how nicotine usurps the cellular mechanisms of synaptic plasticity, (3) the physiological changes in the hippocampus that may contribute to nicotine withdrawal deficits in learning, and (4) the role of genetics and developmental stage (i.e., adolescence) in these effects.
AB - Addiction is a chronic disorder marked by long-lasting maladaptive changes in behavior and in reward system function. However, the factors that contribute to the behavioral and biological changes that occur with addiction are complex and go beyond reward. Addiction involves changes in cognitive control and the development of disruptive drug-stimuli associations that can drive behavior. A reason for the strong influence drugs of abuse can exert on cognition may be the striking overlap between the neurobiological substrates of addiction and of learning and memory, especially areas involved in declarative memory. Declarative memories are critically involved in the formation of autobiographical memories, and the ability of drugs of abuse to alter these memories could be particularly detrimental. A key structure in this memory system is the hippocampus, which is critically involved in binding multimodal stimuli together to form complex long-term memories. While all drugs of abuse can alter hippocampal function, this review focuses on nicotine. Addiction to tobacco products is insidious, with the majority of smokers wanting to quit; yet the majority of those that attempt to quit fail. Nicotine addiction is associated with the presence of drug-context and drug-cue associations that trigger drug seeking behavior and altered cognition during periods of abstinence, which contributes to relapse. This suggests that understanding the effects of nicotine on learning and memory will advance understanding and potentially facilitate treating nicotine addiction. The following sections examine: (1) how the effects of nicotine on hippocampus-dependent learning change as nicotine administration transitions from acute to chronic and then to withdrawal from chronic treatment and the potential impact of these changes on addiction, (2) how nicotine usurps the cellular mechanisms of synaptic plasticity, (3) the physiological changes in the hippocampus that may contribute to nicotine withdrawal deficits in learning, and (4) the role of genetics and developmental stage (i.e., adolescence) in these effects.
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U2 - 10.1016/j.nlm.2013.08.004
DO - 10.1016/j.nlm.2013.08.004
M3 - Review article
C2 - 23973448
AN - SCOPUS:84891560664
SN - 1074-7427
VL - 107
SP - 108
EP - 132
JO - Neurobiology of Learning and Memory
JF - Neurobiology of Learning and Memory
ER -