Nicotine increases FosB expression within a subset of reward- and memory-related brain regions during both peri- and post-adolescence

Soderstrom, Ken; Qin, Weixi; Williams, Helen L.; Taylor, David A.; McMillen, Brian A.

doi:10.1007/s00213-007-0744-9

Cited by 20 publications

(14 citation statements)

References 25 publications

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“…In line with this, several authors have shown that acute NIC (Salminen et al, 1996), chronic NIC (Soderstrom et al, 2007), NIC self-administration (Pagliusi et al, 1996) and NIC rewarding effects (Mombereau et al, 2007) induced an increase in Fos-like immunoreactivity in diverse brain regions. c-Fos is a transcription factor considered to be a marker of neuronal activity (Dragunow and Faull, 1989).…”

Section: Discussionmentioning

confidence: 70%

Acute behavioural responses to nicotine and nicotine withdrawal syndrome are modified in GABAB1 knockout mice

et al. 2012

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Section: Discussionmentioning

confidence: 70%

Acute behavioural responses to nicotine and nicotine withdrawal syndrome are modified in GABAB1 knockout mice

et al. 2012

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“…Chronic nicotine produces a complex set of changes in phosphorylation [132] and expression of immediate early genes [133][134][135][136], perhaps most notably in NAc. Persistent increases in FosB expression were observed in NAc of rats following periadolescant nicotine exposure [136].…”

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confidence: 99%

“…Persistent increases in FosB expression were observed in NAc of rats following periadolescant nicotine exposure [136]. Accumulation of a long-lived truncated form of FosB, deltaFosB, following drug administration (including nicotine) [135] has been proposed as a sustained molecular change that contributes to the persistence of drug dependence and the propensity to relapse [137].…”

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confidence: 99%

Nicotinic acetylcholine receptors and the ascending dopamine pathways

Livingstone

Wonnacott

2009

Biochemical Pharmacology

123

114

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Nicotinic acetylcholine receptors (nAChRs) are widely expressed in midbrain dopamine neurons that project to dorsal striatum, nucleus accumbens and prefrontal cortex. Thus nAChRs can influence the functions of these three pathways; notably motor control, 'reward' and executive function, respectively. Diverse subtypes of nAChRs have been identified on dopamine cell bodies and terminals as well as on neighbouring afferents and interneurons. Here we review the molecular and cellular mechanisms through which nAChRs exert their influence on these pathways in rodents. Page 4 of 40A c c e p t e d M a n u s c r i p t A c c e p t e d M a n u s c r i p t 5 IntroductionThe association of nicotine with tobacco addiction has stimulated particular interest in how nicotine interacts with the 'reward' pathways of the brain. Most attention has been given to the ascending dopaminergic pathways that arise in the midbrain and project to aspects of the basal ganglia and prefrontal cortex (PFC; Fig. 1). In addition to mediating the reinforcing properties of addictive substances, dopamine is also central to the fine control of movement governed by the basal ganglia, whereas its actions in the PFC are critically important to 'executive' function [1,2]. This includes working memory, behavioural flexibility and decision making, and the PFC is also involved with the anticipation of reward [3,4]. FIGURE ONE NEAR HERENicotine interacts with the dopamine systems via nicotinic acetylcholine receptors (nAChRs), a family of ligand-gated pentameric cation channels constituted from at least nine α and β subunits (α2-7 and β2-4) expressed in the mammalian brain [5]. nAChR subtypes can differ in their sensitivities to nicotine or acetylcholine (ACh), their channel characteristics (including their propensity to desensitise) and their cellular distribution. A high relative permeability to Ca 2+ , a notable characteristic of the α7 nAChR subtype, enables nAChRs to interface with a variety of intracellular Ca 2+ -dependent mechanisms [6]. The localisation of nAChRs on dopamine cell bodies in the ventral tegmental area (VTA) or substantia nigra pars compacta (SNc) allows nicotine to directly modulate dopaminergic cell firing. Additionally, nAChRs on dopamine terminals can influence transmitter release. nAChRs present on afferents projecting to the VTA and SNc or to the terminal fields can also influence the activity of dopaminergic neurons. The nicotinic modulation of dopamine release has generated interest in nAChRs as therapeutic targets for conditions involving dopaminergic dysfunction, including schizophrenia, attention deficit hyperactivity disorder, Parkinson's disease, Alzheimer's disease and age-related cognitive impairment [7][8][9][10].In this review we focus on the mechanisms through which nAChRs modulate the activity of dopamine neurones of the principal ascending pathways (Fig. 1). We will considerPage 6 of 40A c c e p t e d M a n u s c r i p t 6 nicotinic influences on somatodendritic and terminal fields, with the aim of integratin...

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“…Results show a clear increase in ΔFosB levels in the vStr and PFC from both groups of rats following 8 days of adolescent nicotine exposure, but this effect persisted into adulthood only in brain from LLA rats. Soderstrom et al [53] demonstrated that 10 days of nicotine exposure (0.4 mg/kg, i.p.) from PND 34–43 increased FosB immunoreactivity in the NAcc at 37 days following the last nicotine injection, but these authors did not specifically measure ΔFosB or characterize the behavioral phenotype of the animals.…”

Section: Discussionmentioning

confidence: 99%

Ethanol conditioned place preference and alterations in ΔFosB following adolescent nicotine administration differ in rats exhibiting high or low behavioral reactivity to a novel environment

Philpot

Engberg

Wecker

2014

Behavioural Brain Research

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This study determined the effects of adolescent nicotine administration on adult alcohol preference in rats exhibiting high or low behavioral reactivity to a novel environment, and ascertained whether nicotine altered ΔFosB in the ventral striatum (vStr) and prefrontal cortex (PFC) immediately after drug administration or after rats matured to adulthood. Animals were characterized as exhibiting high (HLA) or low (LLA) locomotor activity in the novel open field on postnatal day (PND) 31 and received injections of saline (0.9%) or nicotine (0.56 mg free base/kg) from PND 35–42. Ethanol-induced conditioned place preference (CPP) was assessed on PND 68 following 8 days conditioning in a biased paradigm; ΔFosB was measured on PND 43 or PND 68. Following adolescent nicotine exposure, HLA animals demonstrated a CPP when conditioned with ethanol; LLA animals were unaffected. Further, adolescent nicotine exposure for 8 days increased levels of ΔFosB in limbic regions in both HLA and LLA rats, but this increase persisted into adulthood only in LLA animals. Results indicate that adolescent nicotine exposure facilitates the establishment of an ethanol CPP in HLA rats, and that sustained elevations in ΔFosB are not necessary or sufficient for the establishment of an ethanol CPP in adulthood. These studies underscore the importance of assessing behavioral phenotype when determining the behavioral and cellular effects of adolescent nicotine exposure.

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Nicotine increases FosB expression within a subset of reward- and memory-related brain regions during both peri- and post-adolescence

Abstract: Because this altered gene expression occurs after both peri- and post-adolescent treatment, it cannot be directly responsible for increased consumption and rewarding properties of abused drugs previously established to be distinctly associated with periadolescent nicotine exposure.

Cited by 20 publications

References 25 publications

Acute behavioural responses to nicotine and nicotine withdrawal syndrome are modified in GABAB1 knockout mice

Acute behavioural responses to nicotine and nicotine withdrawal syndrome are modified in GABAB1 knockout mice

Nicotinic acetylcholine receptors and the ascending dopamine pathways

Ethanol conditioned place preference and alterations in ΔFosB following adolescent nicotine administration differ in rats exhibiting high or low behavioral reactivity to a novel environment

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