Evidence for elevated nicotine-induced structural plasticity in nucleus accumbens of adolescent rats

McDonald, Craig G.; Eppolito, Amy K.; Brielmaier, Jennifer; Smith, Liane; Bergstrom, Hadley C.; Lawhead, M.R.; Smith, Robert F.

doi:10.1016/j.brainres.2007.03.019

Cited by 30 publications

(30 citation statements)

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“…Nicotine's effects on nicotinic acetylcholine receptors and regional blood flow in the brain are complex, important, and incompletely understood. Chronic exposure is known to change the structural plasticity of the brain [36,37]. Nicotinic receptor activation acutely causes the release of dopamine, glutamate, norepinephrine, acetylcholine, serotonin, B-endorphin, and gamma-aminobutyric acid (GABA), and acute smoking cessation causes a state of ''subnormal release of dopamine and other neurotransmitters [38].''…”

Section: Discussionmentioning

confidence: 99%

Transdermal Nicotine Replacement Therapy in Cigarette Smokers with Acute Subarachnoid Hemorrhage

et al. 2010

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Despite vasoactive properties, administration of NRT among active smokers with acute SAH appeared to be safe, with similar rates of vasospasm and DCI, and a slightly higher rate of seizures. The association of NRT with lower mortality could be due to chance, to uncontrolled factors, or to a neuroprotective effect of nicotine in active smokers hospitalized with SAH, and should be tested prospectively.

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Section: Discussionmentioning

confidence: 99%

Transdermal Nicotine Replacement Therapy in Cigarette Smokers with Acute Subarachnoid Hemorrhage

et al. 2010

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“…Although these changes in dendritic structure have now been found in several areas, they are not ubiquitous. McDonald et al (2007) reported that, within NAcc, large aspiny neurons were not structurally affected by adolescent nicotine. Bergstrom et al (2008) found that mPFC dendritic alterations were class-specific: adolescent dendritic structure in pyramidal cells with simple apical arbors was unchanged, although basilar dendrites of complex cells were affected.…”

Section: Anatomical Specificity Of Adolescent Nicotine Effectsmentioning

confidence: 98%

“…These data were the first to show that adolescent nicotine exposure resulted in MSN dendritic plasticity in the NAcc shell and that changes in dendritic complexity were selective for more distal locations along the tree. In a subsequent experiment, McDonald et al (2007) used a shorter dosing period (P29-43) and extended analyses to include a comparable adult nicotine dose group, and another cell type within the NAcc, the large cholinergic aspiny neuron. We showed that effects of nicotine on MSN dendritic morphology were detectable at a dose that was insufficient to significantly change dendritic morphology in adult animals.…”

Section: Adolescent Nicotine and Nucleus Accumbens Dendritic Morphologymentioning

confidence: 99%

Adolescent nicotine induces persisting changes in development of neural connectivity

Smith

McDonald

Bergstrom

et al. 2015

Neuroscience & Biobehavioral Reviews

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“…In terms of addiction, drugs of abuse alter the mesolimbic reward pathway, notably at the level of the ventral striatum Bloom, 1988, Self andNestler, 1995), causing changes in MSN morphology and spine density (Russo et al, 2010) as well as the BLA (Bergstrom et al, 2010, Cullen et al, 2013. Specifically, there is evidence for elevated nicotine-induced structural plasticity in nucleus accumbens of adolescent rats (McDonald et al, 2007), where periadolescent nicotine administration produces enduring changes in dendritic morphology of medium spiny neurons from the nucleus accumbens (McDonald et al, 2005) and indeed morphological changes in the accumbens due to many other drugs (Lebedev et al, 2008, Robinson and Kolb, 1999, Peterson et al, 2015, Robinson and Kolb, 2004, Robinson et al, 2001. Also, Bergstrom and colleagues (2010) showed that chronic nicotine exposure reduced dendritic complexity in the BLA, a finding similar to our results.…”

Section: Chapter 5: General Discussionmentioning

confidence: 99%

“…Specifically, there is evidence for elevated nicotine-induced structural plasticity in nucleus accumbens of adolescent rats (McDonald et al, 2007), where periadolescent nicotine administration produces enduring changes in dendritic morphology of medium spiny neurons from the nucleus accumbens (McDonald et al, 2005). Also, morphological changes have been characterized due to exposure to alcohol (Lebedev et al, 2008, Peterson et al, 2015, and various other drugs (Robinson and Kolb, 1999, Robinson et al, 2001, Robinson and Kolb, 2004, Rafols et al, 1989.…”

Section: Morphology Of Neurons In the Nacmentioning

confidence: 99%

The Effects of Binge-Like Sucrose Consumption on the Mesolimbic Reward Pathway in the Brain

Shariff¹

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Obesity is becoming a worldwide epidemic (WHO, 2000, Leigh and Morris, 2016, Lifshitz and Lifshitz, 2014, James, 2004. Pharmacotherapeutics that attempt to stem overweight and obesity have largely been ineffective and often are accompanied by adverse side effects (Glazer, 2001). It is therefore imperative to develop effective strategies to combat obesity. A paradigm that has gained momentum relatively recently is the development of addiction to fat and sweet food (Fortuna, 2012, Smith and Robbins, 2013, Volkow et al., 2013a. While drugs of abuse affect various brain subregions, they have been shown to act on three major areas of the brain, namely the brain stem, the limbic system and the cerebral cortex (NIDA, 2010).The limbic system is an interconnected collection of brain structures such as the nucleus accumbens (NAc) and the basolateral amygdala (BLA), whose neural connectivities encode emotional states such as anticipation of reward and motivation (Berridge, 2012). At the molecular level, in addition to the various dysregulatory outcomes in relation to neurotransmitters, it is the dysregulation of balance between dopamine (DA) and acetylcholine (ACh) in the limbic system, especially in the NAc that has been found to drive and maintain behaviours that perpetuate addiction to substances of abuse (Hoebel et al., 2007, Aosaki et al., 2010. Interestingly, sucrose, a potent contributor to the development of obesity (Lakhan and Kirchgessner, 2013, Tappy et al., 2010), has been shown, albeit indirectly, to affect the release of DA in the NAc via the nAChRs (Avena et al., 2008). The role of specific subtypes of nAChRs in the NAc has yet to be elucidated in relation to sucrose consumption.Firstly, this study establishes that the nAChRs are involved in regulating sucrose consumption. Based on the various nAChRs agonists/partial agonists and antagonists tested systemically, it is surmised that *nAChRs are involved in mediating sucrose consumption.Furthermore, coupled to the changes in nAChRs, this study also sheds light for the first time ii on the global morphological changes that occur in the dendrites of the neurons in the NAc and BLA reminiscent of similar changes due to drugs of abuse, suggestive of a global imbalance at the level of the NAc and amygdala. Further studies are warranted to determine the precise functional significance of the morphological changes that are reported in this study, and to discover potential newer pharmacotherapies that target the nAChRs. At the present time, however, varenicline, an FDA approved pharmacotherapeutic, appears to be an attractive agent in reducing sucrose intake. Varenicline may hold potential benefits in lowering weight gain thus concomitantly lowering the global burden of obesity-related disease.iii

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Evidence for elevated nicotine-induced structural plasticity in nucleus accumbens of adolescent rats

Cited by 30 publications

References 31 publications

Transdermal Nicotine Replacement Therapy in Cigarette Smokers with Acute Subarachnoid Hemorrhage

Transdermal Nicotine Replacement Therapy in Cigarette Smokers with Acute Subarachnoid Hemorrhage

Adolescent nicotine induces persisting changes in development of neural connectivity

The Effects of Binge-Like Sucrose Consumption on the Mesolimbic Reward Pathway in the Brain

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