Donepezil reverses nicotine withdrawal-induced deficits in contextual fear conditioning in c57bl/6j mice.

Poole, Rachel L.; Connor, David A.; Gould, Thomas J.

doi:10.1037/bne0000003

Cited by 11 publications

(11 citation statements)

References 49 publications

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“…Acute nicotine treatment reverses the impairment produced by nicotine withdrawal on contextual fear conditioning (Davis et al, 2005), as do other putative or current nicotine cessation treatments, including bupropion (Portugal and Gould, 2007), varenicline (Raybuck et al, 2008), donepezil (Poole et al, 2014) and galantamine (Wilkinson and Gould, 2011). The deficits in contextual fear conditioning in these studies has been compared to cognitive deficits in ADHD and are reversed by atomoxetine (Davis and Gould, 2007a).…”

Section: Animal Models Of Nicotine Dependence: Withdrawal Effects On mentioning

confidence: 97%

Negative affective states and cognitive impairments in nicotine dependence

Hall

Der-Avakian

Gould

et al. 2015

Neuroscience & Biobehavioral Reviews

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Smokers have substantial individual differences in quit success in response to current treatments for nicotine dependence. This observation may suggest that different underlying motivations for continued tobacco use across individuals and nicotine cessation may require different treatments in different individuals. Although most animal models of nicotine dependence emphasize the positive reinforcing effects of nicotine as the major motivational force behind nicotine use, smokers generally report that other consequences of nicotine use, including the ability of nicotine to alleviate negative affective states or cognitive impairments, as reasons for continued smoking. These states could result from nicotine withdrawal, but also may be associated with premorbid differences in affective and/or cognitive function. Effects of nicotine on cognition and affect may alleviate these impairments regardless of their premorbid or postmorbid origin (e.g., before or after the development of nicotine dependence). The ability of nicotine to alleviate these symptoms would thus negatively reinforce behavior, and thus maintain subsequent nicotine use, contributing to the initiation of smoking, the progression to dependence and relapse during quit attempts. The human and animal studies reviewed here support the idea that self-medication for pre-morbid and withdrawal-induced impairments may be more important factors in nicotine addiction and relapse than has been previously appreciated in preclinical research into nicotine dependence. Given the diverse beneficial effects of nicotine under these conditions, individuals might smoke for quite different reasons. This review suggests that inter-individual differences in the diverse effects of nicotine associated with self-medication and negative reinforcement are an important consideration in studies attempting to understand the causes of nicotine addiction, as well as in the development of effective, individualized nicotine cessation treatments.

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Section: Animal Models Of Nicotine Dependence: Withdrawal Effects On mentioning

confidence: 97%

Negative affective states and cognitive impairments in nicotine dependence

Hall

Der-Avakian

Gould

et al. 2015

Neuroscience & Biobehavioral Reviews

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“…Enhanced cognitive performance following acute nicotine exposure has also been seen in rodent models of attention (Hahn et al 2002). Conversely, nicotine withdrawal produces impairments in both contextual learning and attention-based models (Semenova et al 2007;Gould et al 2012;Portugal et al 2012;Poole et al 2014;Yildirim et al 2015). From these studies, it is apparent that nicotine alters cognitive function in adults depending on multiple factors including duration of treatment.…”

Section: Nicotinementioning

confidence: 98%

The long-term cognitive consequences of adolescent exposure to recreational drugs of abuse

Mooney‐Leber

Gould

2018

Learn. Mem.

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During adolescence, the brain continues to undergo vital developmental processes. In turn, complex behavioral and cognitive skills emerge. Unfortunately, neurobiological development during adolescence can be influenced by environmental factors such as drug exposure. Engaging in drug use during adolescence has been a long-standing health concern, especially how it predicts or relates to drug using behavior later in life. However, recent findings suggest that other behavioral domains, such as learning and memory, are also vulnerable to adolescent drug use. Moreover, it is becoming increasingly apparent that deficits in learning and memory following adolescent drug use endure into adulthood, well after drug exposure has subsided. Although persistent effects suggest an interaction between drug exposure and ongoing development during adolescence, the exact acute and long-term consequences of adolescent drug exposure on substrates of learning and memory are not fully understood. Thus, this review will summarize human and animal findings on the enduring cognitive deficits due to adolescent drug exposure. Moreover, due to the fact that adolescents are more likely to consume drugs of abuse legally available to adults, this review will focus on alcohol, nicotine, and marijuana. Further, given the critical role of the frontal cortex and hippocampus in various learning and memory domains, the impact adolescent use of the previous listed drugs on the neurobiology within these regions will also be discussed.

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“…Decreased contextual fear responses were seen in mice during spontaneous or precipitated nicotine withdrawal, and this reduction during nicotine withdrawal was not seen in mice lacking the β2 nAChR subunit (Portugal et al, ). Nicotine withdrawal effects are also reversed with the α4β2‐selective partial agonists ABT‐089 and varenicline as well as acetylcholinesterase inhibitors such as donepezil and galantamine (Raybuck et al, ; Wilkinson and Gould, ; Poole et al, ; Yildirim et al, ). Much higher doses of donepezil or galantamine were required to enhance conditioned fear responses in nondependent animals, and these effects were associated with enhanced acquisition of conditioned responses and/or unconditioned freezing (Wilkinson and Gould, ; Poole et al, ).…”

Section: Cholinergic Regulation Of Contextual Fear Responsesmentioning

confidence: 99%

“…Nicotine withdrawal effects are also reversed with the α4β2‐selective partial agonists ABT‐089 and varenicline as well as acetylcholinesterase inhibitors such as donepezil and galantamine (Raybuck et al, ; Wilkinson and Gould, ; Poole et al, ; Yildirim et al, ). Much higher doses of donepezil or galantamine were required to enhance conditioned fear responses in nondependent animals, and these effects were associated with enhanced acquisition of conditioned responses and/or unconditioned freezing (Wilkinson and Gould, ; Poole et al, ). Thus, although nicotine can modify contextual fear responses, only a few studies have shown effects of nAChR antagonists or acetylcholinesterase inhibitors (see Table ).…”

Section: Cholinergic Regulation Of Contextual Fear Responsesmentioning

confidence: 99%

Cholinergic regulation of fear learning and extinction

Wilson

Fadel

2016

J of Neuroscience Research

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Cholinergic activation regulates cognitive function, and particularly long term memory consolidation. Here we present an overview of the anatomical, neurochemical, and pharmacological evidence supporting the cholinergic regulation of Pavlovian contextual and cue conditioned fear learning and extinction. Basal forebrain cholinergic neurons provide inputs to neocortical regions and subcortical limbic structures such as the hippocampus and amygdala. Pharmacological manipulations of muscarinic and nicotinic receptors support the role of cholinergic processes in the amygdala, hippocampus, and prefrontal cortex in modulating the learning and extinction of contexts or cues associated with threat. Additional evidence from lesion studies and analysis of in vivo acetylcholine release using microdialysis similarly support a critical role of cholinergic neurotransmission in cortico-amygdalar or cortico-hippocampal circuits during acquisition of fear extinction. Although a few studies suggest a complex role of cholinergic neurotransmission in the cellular plasticity needed for extinction learning, more work is needed to elucidate the exact cholinergic mechanisms and physiological role of muscarinic and nicotinic receptors in these fear circuits. Such studies will be important for elucidating the role of cholinergic neurotransmission in disorders such as post-traumatic stress disorder (PTSD) that involve deficits in extinction learning as well as developing novel therapeutic approaches for such disorders.

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Donepezil reverses nicotine withdrawal-induced deficits in contextual fear conditioning in c57bl/6j mice.

Cited by 11 publications

References 49 publications

Negative affective states and cognitive impairments in nicotine dependence

Negative affective states and cognitive impairments in nicotine dependence

The long-term cognitive consequences of adolescent exposure to recreational drugs of abuse

Cholinergic regulation of fear learning and extinction

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