Nicotine-Induced Limbic Cortical Activation in the Human Brain: A Functional MRI Study

Stein, Elliot A.; Pankiewicz, John; Harsch, Harold H.; Cho, Jung Ki; Fuller, Scott A.; Hoffmann, Raymond G.; Hawkins, Marjorie; Rao, Stephen M.; Bandettini, Peter A.; Bloom, Alan S.

doi:10.1176/ajp.155.8.1009

Cited by 443 publications

(292 citation statements)

References 28 publications

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“…The dose of nicotine administered might also have been a contributor to the small change in BP we observed. We elected to keep the dose of nicotine around 0.03 mg/kg, because this was a dose that Stein et al (1998) reported to be well tolerated when administered as a 1 min i.v. bolus in human smokers (a cigarette contains between 0.01 and 0.03 mg/kg nicotine for a 70 kg person).…”

Section: Discussionmentioning

confidence: 99%

“…Although there was no statistically significant difference between the two methods of tracer administration (B/I and bolus), we believe the B/I technique offers some advantages: it is more economical because it provides the same information with a single [ 11 C]raclopride synthesis; calculation of BP images is simplified; values outside the immediate area of the basal ganglia are less noisy than with images created with SRTM, potentially enabling analysis of BP changes over the whole brain; even within the basal ganglia the statistical quality of the images is improved; and it is less sensitive to changes in blood flow (Carson, 2000) induced by nicotine (Domino et al, 2000;Stein et al, 1998;Zubieta et al, 2001). Although these arguments support the use of the B/I method for studies of nicotine-induced DA release, this decision has to be weighted according to the characteristics of the tracer and the displacement expected.…”

Section: Discussionmentioning

confidence: 99%

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Nicotine-Induced Dopamine Release in Primates Measured with [11C]Raclopride PET

Marenco¹,

Carson²,

Berman³

et al. 2003

Neuropsychopharmacol

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Nicotine-induced dopamine (DA) release constitutes a pharmacological probe of the DA system that has potential use in patients with schizophrenia, who have abnormally elevated DA release after amphetamine administration and possibly abnormalities in nicotinic signaling. We performed positron emission tomography studies in five rhesus monkeys that received i.v. nicotine doses ranging from 0.01 to 0.06 mg/kg. [ 11 C]raclopride was administered with either a bolus plus constant infusion or with paired bolus injections. The dynamics of D-2-binding potential (BP) after nicotine administration were studied and compared to amphetamine. Nicotine caused a significant albeit small reduction (5%, po0.03) in BP, regardless of methodology of tracer administration. This effect disappeared 2.5 h after nicotine administration. Amphetamine caused much larger and prolonged displacement of [ 11 C]raclopride as compared to nicotine. There was no correlation between changes in BP and nicotine dose or plasma level. Regional differences in the nicotine effect within the basal ganglia were not found. Our data are consistent with the increase in DA detected with microdialysis in animals after acute nicotine administration, however, a larger effect size would be desirable to attempt studies comparing human smokers with and without schizophrenia.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Nicotine-Induced Dopamine Release in Primates Measured with [11C]Raclopride PET

Marenco¹,

Carson²,

Berman³

et al. 2003

Neuropsychopharmacol

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“…In studies examining regional activity responses to nicotine or smoking, the most common findings are relative increases in activity in the prefrontal cortex (including the dorsolateral prefrontal cortex, and inferior frontal, medial frontal, and orbitofrontal gyri) (Domino et al, 2000b;Rose et al, 2003;Stein et al, 1998), thalamus (Domino et al, 2000a;Domino et al, 2000b;London et al, 1988a,b;Stein et al, 1998;Zubieta et al, 2001), and visual system (Domino et al, 2000a;Domino et al, 2000b;London et al, 1988a,b) (Jed Rose, Personal Communication). Additionally, a Xe 133 inhalation study reported increases in frontal lobe and thalamic blood flow in smokers who smoked a cigarette (Nakamura et al, 2000).…”

Section: Brain Activity Responses To Nicotine/cigarette Administrationmentioning

confidence: 99%

Functional brain imaging of tobacco use and dependence

Brody

2006

Journal of Psychiatric Research

176

136

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While most cigarette smokers endorse a desire to quit smoking, only about 14% to 49% will achieve abstinence after 6 months or more of treatment. A greater understanding of the effects of smoking on brain function may (in conjunction with other lines of research) result in improved pharmacological (and behavioral) interventions. Many research groups have examined the effects of acute and chronic nicotine/cigarette exposure on brain activity using functional imaging; the purpose of this paper is to synthesize findings from such studies and present a coherent model of brain function in smokers. Responses to acute administration of nicotine/smoking include: a reduction in global brain activity; activation of the prefrontal cortex, thalamus, and visual system; activation of the thalamus and visual cortex during visual cognitive tasks; and increased dopamine (DA) concentration in the ventral striatum/nucleus accumbens. Responses to chronic nicotine/cigarette exposure include decreased monoamine oxidase (MAO) A and B activity in the basal ganglia and a reduction in α 4 β 2 nicotinic acetylcholine receptor (nAChR) availability in the thalamus and putamen. Taken together, these findings indicate that smoking enhances neurotransmission through cortico-basal ganglia-thalamic circuits either by direct stimulation of nAChRs, indirect stimulation via DA release or MAO inhibition, or a combination of these factors. Activation of this circuitry may be responsible for the effects of smoking seen in tobacco dependent subjects, such as improvements in attentional performance, mood, anxiety, and irritability.

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“…In pharmacological fMRI studies to date, the temporal profile of the drug's effect has been assumed. The assumption has either been implicit in comparing fMRImeasured brain activity before and after administration (Breiter et al, 1997;Coull et al, 2001;Furey et al, 2000;Hariri et al, 2002;Honey et al, 1999;Kimberg et al, 2001;Kleinschmidt et al, 1999;Mattay et al, 2000;Thiel et al, 2001Thiel et al, , 2002, or the assumption has been more explicit in incorporating pre-existing pharmacokinetic parameters into the analysis of fMRI data (Stein et al, 1998;Bloom et al, 1999;Wise et al, 2002). In either case, the aim has been to simply identify drug-induced changes in brain activity.…”

Section: Introductionmentioning

confidence: 99%

Using fMRI to Quantify the Time Dependence of Remifentanil Analgesia in the Human Brain

Wise

Williams

Tracey

2003

Neuropsychopharmacol

108

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To understand and exploit centrally acting drugs requires reliable measures of their time course of action in the human brain. Functional magnetic resonance imaging (fMRI) is able to measure noninvasively, drug-induced changes in task-related brain activity. Here, we have characterized, in a specific region of the brain, the time of onset of action and the half-life of action of a clinically relevant dose of a potent opioid analgesic agent, remifentanil. These times were established from the temporal variation of the amplitude of the blood oxygen level-dependent response in the insular cortex contralateral to a painfully hot thermal stimulus, in volunteers receiving a remifentanil infusion. The insular cortex has repeatedly been reported as activated by noxious thermal stimulation. The times of onset and offset of drug action were each characterized by a half-life for changes in fMRI signal from within the insula. These characteristic times agreed with the observed drug-induced analgesia and previous pharmacokinetic-pharmacodynamic measurements for remifentanil. We have successfully measured, for the first time using fMRI, temporal pharmacological parameters for a CNS-active drug based on its effect on task-related activity in a specific brain region. Comparison of the time course of regional brain activity with pain perception could reveal those regions engaged in drug-induced analgesia.

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Nicotine-Induced Limbic Cortical Activation in the Human Brain: A Functional MRI Study

Cited by 443 publications

References 28 publications

Nicotine-Induced Dopamine Release in Primates Measured with [11C]Raclopride PET

Nicotine-Induced Dopamine Release in Primates Measured with [11C]Raclopride PET

Functional brain imaging of tobacco use and dependence

Using fMRI to Quantify the Time Dependence of Remifentanil Analgesia in the Human Brain

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