A comparison of the effects of nicotine on dopamine and non-dopamine neurons in the rat ventral tegmental area: an in vitro electrophysiological study

Yin, Ruoyuan; French, Edward D.

doi:10.1016/s0361-9230(00)00237-9

Cited by 81 publications

(58 citation statements)

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“…GABAergic inputs to the VTA DA neurons come from local interneurons and from projection fibers from the NAcc and the ventral pallidum (Walaas and Fonnum, 1980;Kalivas et al, 1993;Steffensen et al, 1998). When nicotine reaches the VTA, nAChRs expressed by GABA neurons in the nucleus are activated and cause an increase in the firing rate of these neurons (Yin and French, 2000;Mansvelder et al, 2002). These nAChRs are mostly of the non-␣7 type that likely contain ␣4 and ␤2 subunits.…”

Section: Nicotinic Modulation Of Gabaergic Transmission In the Vtamentioning

confidence: 99%

Cellular and synaptic mechanisms of nicotine addiction

2002

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ABSTRACT:The tragic health effects of nicotine addiction highlight the importance of investigating the cellular mechanisms of this complex behavioral phenomenon. The chain of cause and effect of nicotine addiction starts with the interaction of this tobacco alkaloid with nicotinic acetylcholine receptors (nAChRs). This interaction leads to activation of reward centers in the CNS, including the mesoaccumbens DA system, which ultimately leads to behavioral reinforcement and addiction. Recent findings from a number of laboratories have provided new insights into the biologic processes that contribute to nicotine self-administration.Examination of the nAChR subtypes expressed within the reward centers has identified potential roles for these receptors in normal physiology, as well as the effects of nicotine exposure. The high nicotine sensitivity of some nAChR subtypes leads to rapid activation followed in many cases by rapid desensitization. Assessing the relative importance of these molecular phenomena in the behavioral effects of nicotine presents an exciting challenge for future research efforts.

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Section: Nicotinic Modulation Of Gabaergic Transmission In the Vtamentioning

confidence: 99%

Cellular and synaptic mechanisms of nicotine addiction

2002

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“…Nicotine has been shown to directly activate these neurons (Pidoplichko et al, 1997,Yin andFrench, 2000). Moreover, nicotine stimulates release of DA within the striatal target region by direct action on nicotinic receptors on DA terminals (Rapier et al, 1990,Grady et al, 1992,Clarke and Reuben, 1996,Wonnacott, 1997.…”

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confidence: 99%

Developmental regulation of nicotinic acetylcholine receptors within midbrain dopamine neurons

2007

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We have combined anatomical and functional methodologies to provide a comprehensive analysis of the properties of nicotinic acetylcholine receptors (nAChRs) on developing dopamine (DA) neurons. Double-labeling in situ hybridization was used to examine the expression of nAChR subunit mRNAs within developing midbrain DA neurons. As brain maturation progressed there was a change in the pattern of subunit mRNA expression within DA neurons, such that α3 and α4 subunits declined and α6 mRNA increased. Although there were strong similarities in subunit mRNA expression in substantia nigra (SNc) and ventral tegmental area (VTA), there was higher expression of α4 mRNA in SNc than VTA at gestational day (G)15, and of α5, α6 and β3 mRNAs during postnatal development. Using a superfusion neurotransmitter release paradigm to functionally characterize nicotine-stimulated release of [ 3 H]DA from striatal slices, the properties of the nAChRs on DA terminals were also found to change with age. Functional nAChRs were detected on striatal terminals at G18. There was a decrease in maximal release in the first postnatal week, followed by an increase in nicotine efficacy and potency during the second and third postnatal weeks. In the transition from adolescence (postnatal days (P) 30 and 40) to adulthood, there was a complex pattern of functional maturation of nAChRs in ventral, but not dorsal, striatum. In males, but not females, there were significant changes in both nicotine potency and efficacy during this developmental period. These findings suggest that nAChRs may play critical functional roles throughout DA neuronal maturation. Keywords adolescent; fetal; nicotine; sex; striatum; maternal smoking Maternal smoking during pregnancy has been correlated with a number of adverse outcomes in the offspring (Lichtensteiger et al., 1988,Lichtensteiger andSchlumpf, 1993), including cognitive deficits that are often manifested in early childhood as attention deficit hyperactivity disorder (ADHD) (Millberger et al., 1996). Though the underlying neurobiological mechanism * Correspondence to: Dr. Layla Azam Department of Biology, University of Utah 257 South 1400 East Salt Lake City, UT 84112 Tel.: (801) Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. ,Pliszka et al., 1996,Castellanos, 1997. In animal studies, maternal nicotine exposure produces sexdependent alterations in the development of DA neurochemical markers (Fung, 1988,Fung, 1989,Ribary and Lichtensteiger, 1989,Lichtensteiger and Schlumpf, 1993,Muneoka et al., 1997, and induces hyperactivity in the offspring, which is believed...

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“…Notably, evidence from humanand animal-based research implicates the mesolimbic dopamine (DA) system, comprising the ventral tegmental area (VTA) and its projections to the nucleus accumbens (NAc) core (NAcore) and shell (NAshell) subregions, as important regulators of nicotine's motivational properties (Picciotto and Corrigall, 2002;Laviolette and van der Kooy, 2004). The importance of DA neurotransmission in nicotine's motivational effects is further underscored by evidence showing that DA release is strongly increased by nicotine, by directly exciting VTA DAergic neurons and/or increasing release of DA in the terminal fields of the mesolimbic DAergic projections (Nisell et al, 1994;Yin and French, 2000;Mansvelder and McGehee, 2002). Furthermore, nicotine can act directly within the VTA to produce motivational effects (Laviolette and van der Kooy, 2003;David et al, 2006;Ikemoto et al, 2006) through either DA-dependent or non-DAergic neural systems (Picciotto et al, 1998; van der Kooy, 2003, 2004).…”

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Dopamine Signaling through D₁-Like versus D₂-Like Receptors in the Nucleus Accumbens Core versus Shell Differentially Modulates Nicotine Reward Sensitivity

Laviolette¹,

Lauzon²,

Bishop³

et al. 2008

J. Neurosci.

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Considerable evidence implicates the mesolimbic dopamine (DA) system in the processing of nicotine's reinforcing properties, specifically the ventral tegmental area (VTA) and the terminal fields of VTA DAergic projections to the "core" (NAcore) and "shell" (NAshell) subdivisions of the nucleus accumbens (NAc). However, the specific roles of DA D 1 -like and D 2 -like receptor subtypes in nicotine reward processing within these NAc subregions have not been elucidated. We report that microinfusions of DA D 1 -like or D 2 -like receptorspecific antagonists into NAcore or NAshell double dissociate the rewarding and aversive properties of systemic or intra-VTA nicotine, and differentially regulate sensitivity to the rewarding properties as well as the motivational valence of either intra-VTA or systemic nicotine administration. Using a place conditioning procedure, NAshell infusions of a D 2 -like receptor antagonist switched the motivational valence of intra-VTA nicotine from aversive to rewarding and potentiated nicotine reward sensitivity to sub-reward threshold intra-VTA nicotine doses. In contrast, NAcore infusions of a D 1 -like receptor antagonist switched intra-VTA nicotine aversion to reward, and potentiated reward sensitivity to sub-reward threshold nicotine doses. Thus, D 1 -like versus D 2 -like receptors in NAcore versus NAshell subdivisions play functionally dissociable roles in modulating systemic or intra-VTA nicotine motivational processing.Key words: nicotine; addiction; dopamine; ventral tegmental area; receptors; nucleus accumbens IntroductionNicotine, the psychoactive component of tobacco smoke, produces a variety of motivational effects and has strong addictive properties. Several neural regions and neurotransmitter systems have been implicated as critical mediators of nicotine's dependence-producing effects. Notably, evidence from humanand animal-based research implicates the mesolimbic dopamine (DA) system, comprising the ventral tegmental area (VTA) and its projections to the nucleus accumbens (NAc) core (NAcore) and shell (NAshell) subregions, as important regulators of nicotine's motivational properties (Picciotto and Corrigall, 2002;Laviolette and van der Kooy, 2004). The importance of DA neurotransmission in nicotine's motivational effects is further underscored by evidence showing that DA release is strongly increased by nicotine, by directly exciting VTA DAergic neurons and/or increasing release of DA in the terminal fields of the mesolimbic DAergic projections (Nisell et al., 1994;Yin and French, 2000;Mansvelder and McGehee, 2002). Furthermore, nicotine can act directly within the VTA to produce motivational effects (Laviolette and van der Kooy, 2003;David et al., 2006;Ikemoto et al., 2006) through either DA-dependent or non-DAergic neural systems (Picciotto et al., 1998; van der Kooy, 2003, 2004). Like many drugs of abuse, nicotine possesses both reinforcing and aversive stimulus properties, and nicotine dosedependently produces rewarding or aversive effects directly within the VTA w...

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A comparison of the effects of nicotine on dopamine and non-dopamine neurons in the rat ventral tegmental area: an in vitro electrophysiological study

Cited by 81 publications

References 43 publications

Cellular and synaptic mechanisms of nicotine addiction

Cellular and synaptic mechanisms of nicotine addiction

Developmental regulation of nicotinic acetylcholine receptors within midbrain dopamine neurons

Dopamine Signaling through D₁-Like versus D₂-Like Receptors in the Nucleus Accumbens Core versus Shell Differentially Modulates Nicotine Reward Sensitivity

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A comparison of the effects of nicotine on dopamine and non-dopamine neurons in the rat ventral tegmental area: an in vitro electrophysiological study

Cited by 81 publications

References 43 publications

Cellular and synaptic mechanisms of nicotine addiction

Cellular and synaptic mechanisms of nicotine addiction

Developmental regulation of nicotinic acetylcholine receptors within midbrain dopamine neurons

Dopamine Signaling through D1-Like versus D2-Like Receptors in the Nucleus Accumbens Core versus Shell Differentially Modulates Nicotine Reward Sensitivity

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Dopamine Signaling through D₁-Like versus D₂-Like Receptors in the Nucleus Accumbens Core versus Shell Differentially Modulates Nicotine Reward Sensitivity