Common Neural Substrates for the Addictive Properties of Nicotine and Cocaine

  title={Common Neural Substrates for the Addictive Properties of Nicotine and Cocaine},
  author={Emilio Merlo Pich and Sonia R. Pagliusi and Michela A. Tessari and Dominique Talabot-Ayer and Rob Hooft van Huijsduijnen and Christian Chiamulera},
  pages={83 - 86}
Regional brain activation was assessed by mapping of Fos-related protein expression in rats trained to self-administration of intravenous nicotine and cocaine. Both drugs produced specific overlapping patterns of activation in the shell and the core of the nucleus accumbens, medial prefrontal cortex, and medial caudate areas, but not in the amygdala. Thus, the reinforcing properties of cocaine and nicotine map on selected structures of the terminal fields of the mesocorticolimbic dopamine… 
Neural substrate of nicotine addiction as defined by functional brain maps of gene expression
Post-mortem brain maps of c-fos-related antigens expression showed specific activation in prefrontal cortex, anterior cingulate and nucleus accumbens for both drugs, but of the anterior cedulate cortex only during relapse, suggesting that a subset of the neural network involved in drug self-administration is activated during relapse.
Modulation of ventral tegmental area dopamine receptors inhibit nicotine-induced anxiogenic-like behavior in the central amygdala
The relationship between the VTA and the CeA may be involved in nicotine-induced anxiogenic-like behavior via dopamine D(1) and D(2)/(3) receptors, which will be crucial for the development of new intervention to combat nicotine effect.
Cocaine-predictive stimulus induces drug-seeking behavior and neural activation in limbic brain regions after multiple months of abstinence: reversal by D(1) antagonists.
The undiminished efficacy of the cocaine S(D) to elicit drug-seeking behavior after 4 months of abstinence parallels the long-lasting nature of conditioned cue reactivity and cue-induced cocaine craving in humans, and confirms a significant role of learning factors in the long,lasting addictive potential of cocaine.
Nicotine self-administration in animals as a dependence model.
  • W. Corrigall
  • Medicine
    Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco
  • 1999
This manuscript describes the use of one particular paradigm, a model in which work is done by laboratory animals to obtain intravenous infusions of nicotine, which is particularly useful for examining the mechanisms in the brain that are responsible for the maintenance of drug-taking behavior.
Role of nicotinic acetylcholine receptors in cerebral dopaminergic transmission and expression of fos protein
Cigarette smoking is the most widespread form of drug abuse due to the addictive properties of nicotine present in tobacco. Via binding to specific receptors, known as nicotinic acetylcholine
Response of nicotine self-administration in the rat to manipulations of mu-opioid and γ-aminobutyric acid receptors in the ventral tegmental area
The lesser effect of DAMGO microinfusions in the VTA on nicotine than cocaine self-administration is associated with the opposite efficacy of GABA agonists, suggesting that nicotine and cocaine differentially activate circuitry in which mu receptors are situated.
Functional correlates of nicotine administration: similarity with drugs of abuse
The results demonstrate that nicotine shares with highly addictive drugs a distinct neurochemical and functional consequence that contribute to the neurochemical definition of the addictive nature of nicotine.
Differential Desensitization and Distribution of Nicotinic Acetylcholine Receptor Subtypes in Midbrain Dopamine Areas
The results suggest that nicotine, as obtained from tobacco, can have multiple effects on the midbrain areas by differentially influencing dopamine neurons of the VTA and SNc and differentially desensitizing α7* and non-α7 nAChRs.
Alpha7-nicotinic receptors modulate nicotine-induced reinforcement and extracellular dopamine outflow in the mesolimbic system in mice
The present results reveal new insights for the role of α7*nAChRs in modulating the action of nicotine within the mesolimbic circuit, which appear to potentiate the reinforcing action of Nicotine administered into the VTA while regulating its action over time on DA outflow in the ACb.
Elevations of FosB in the nucleus accumbens during forced cocaine abstinence correlate with divergent changes in reward function
Data indicate that alterations in the expression of FosB-like transcription factors in the NAc can predict the dysregulation of hedonic processing that occurs during protracted withdrawal from cocaine.


Cortical dopaminergic involvement in cocaine reinforcement.
Neuronal systems involved in the initiation of cocaine reinforcement were investigated by identifying brain sites where direct application of the drug was reinforcing. This was accomplished by
Systemic nicotine‐induced dopamine release in the rat nucleus accumbens is regulated by nicotinic receptors in the ventral tegmental area
The results suggest that nicotinic receptors in the somatodendritic region may be of greater importance than those located in the terminal area for the stimulatory action of systemic NIC on the mesolimbic DA system and support the notion that the meslimbic dopaminergic system is phasically rather than tonically regulated by nicotinics receptor activation within the VTA.
Acute nicotine injections induce c-fos mostly in non-dopaminergic neurons of the midbrain of the rat.
It is suggested that acute nicotine injections induce c-fos expression mostly in non-dopaminergic neurons of the ventral tegmental area of the rat and that nicotine induces c- fos most intensely in the interpeduncular nucleus, the superior colliculus, and several other subnuclei of the accessory optic system.
The role of dopamine in drug abuse viewed from the perspective of its role in motivation
Drugs of abuse share with conventional reinforcers the activation of specific neural pathways in the CNS that are the substrate of their motivational properties. Dopamine is recognized as the
Induction of c-fos immunostaining in the rat brain after the systemic administration of nicotine
A subset of central nervous system neurons that respond to nicotine with altered expression of the immediate early gene c-fos is identified, presumably undergoing long-term changes in gene expression as a result of acute exposure to high doses of nicotine.
Cocaine induces striatal c-fos-immunoreactive proteins via dopaminergic D1 receptors.
It is reported that the acute administration of a single dose of the indirect-acting dopaminergic agonist cocaine increases multiple Fos proteins in rat caudate nucleus and this data indicate that D1 dopamine receptors are linked to a cellular immediate-early gene system(s) and suggest an action of cocaine at one or more levels of gene expression via modulation of transcriptional processes in activated cells.
Chronic injections of saline produce subsensitivity to nicotine
The authors report that chronic twice daily injections of normal saline for 14 days produced subsensitivity to the hypothermic effects of nicotine, and propose that this effect reflects the effect of chronic stress on a nicotinic mechanism.
Induction of a long-lasting AP-1 complex composed of altered Fos-like proteins in brain by chronic cocaine and other chronic treatments
The chronic FRAs and associated chronic AP-1 complex could mediate some of the long-term changes in gene expression unique to the chronic-treated state as opposed to the acute-treated and normal states.
Nicotine enhancement of fast excitatory synaptic transmission in CNS by presynaptic receptors.
Findings reveal that CNS nAChRs enhance fast excitatory transmission, providing a likely mechanism for the complex behavioral effects of nicotine.
Expression of c-fos protein in brain: metabolic mapping at the cellular level.
Fos immunohistochemistry provides a cellular method to label polysynaptically activated neurons and thereby map functional pathways in response to polysynaptic activation.