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Article ; Online: The role of the dynorphin-kappa opioid system in the reinforcing effects of drugs of abuse.

Wee, Sunmee / Koob, George F

2010 Volume 210, Issue 2, Page(s) 121–135

Abstract: Background: Initial hypotheses regarding the role of the kappa opioid system in drug addiction suggested that kappa receptor stimulation had anti-addictive effects. However, recent research suggests that kappa receptor antagonists may reverse ... ...

Abstract	Background: Initial hypotheses regarding the role of the kappa opioid system in drug addiction suggested that kappa receptor stimulation had anti-addictive effects. However, recent research suggests that kappa receptor antagonists may reverse motivational aspects of dependence. In the present review, we revisit the studies that measured the effects of kappa receptor ligands on the reinforcing and rewarding effects of drugs and postulate underlying neurobiological mechanisms for these effects to elaborate a more complex view of the role of kappa receptor ligands in drug addiction. Results: The review of studies indicates that kappa receptor stimulation generally antagonizes the acute reinforcing/rewarding effects of drugs whereas kappa receptor blockade has no consistent effect. However, in a drug dependent-like state, kappa receptor blockade was effective in reducing increased drug intake. In animal models of reinstatement, kappa receptor stimulation can induce reinstatement via a stress-like mechanism. Results in conditioned place preference/aversion and intracranial self-stimulation indicate that kappa receptor agonists produce, respectively, aversive-like and dysphoric-like effects. Additionally, preclinical and postmortem studies show that administration or self-administration of cocaine, ethanol, and heroin activate the kappa opioid system. Conclusion: kappa receptor agonists antagonize the reinforcing/rewarding effects of drugs possibly through punishing/aversive-like effects and reinstate drug seeking through stress-like effects. Evidence suggests that abused drugs activate the kappa opioid system, which may play a key role in motivational aspects of dependence. Kappa opioid systems may have an important role in driving compulsive drug intake.
MeSH term(s)	Analgesics, Opioid/pharmacology ; Animals ; Chronic Disease ; Drug Tolerance ; Dynorphins/physiology ; Humans ; Receptors, Opioid, kappa/agonists ; Receptors, Opioid, kappa/antagonists & inhibitors ; Receptors, Opioid, kappa/physiology ; Receptors, Opioid, mu/agonists ; Reinforcement, Psychology ; Reward ; Self Administration ; Substance-Related Disorders/metabolism ; Substance-Related Disorders/psychology
Chemical Substances	Analgesics, Opioid ; Receptors, Opioid, kappa ; Receptors, Opioid, mu ; Dynorphins (74913-18-1)
Language	English
Publishing date	2010-03-30
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	130601-7
ISSN	1432-2072 ; 0033-3158
ISSN (online)	1432-2072
ISSN	0033-3158
DOI	10.1007/s00213-010-1825-8
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Article ; Online: Blockade of TRPV1 Inhibits Methamphetamine-induced Rewarding Effects

Yu-Hua Tian / Shi-Xun Ma / Kwang-Wook Lee / Sunmee Wee / George F. Koob / Seok-Yong Lee / Choon-Gon Jang

Scientific Reports, Vol 8, Iss 1, Pp 1-

2018 Volume 12

Abstract: Abstract Methamphetamine (MAP) is the most widely used psychostimulant in the world, but the exact mechanisms underlying MAP addiction are not yet fully understood. Recent studies have identified the distribution of TRPV1 in several brain regions that ... ...

Abstract	Abstract Methamphetamine (MAP) is the most widely used psychostimulant in the world, but the exact mechanisms underlying MAP addiction are not yet fully understood. Recent studies have identified the distribution of TRPV1 in several brain regions that are related to drug addiction, including nucleus accumbens (NAc) and dorsal striatum (DSt). In the present study, we performed conditioned place preference (CPP) and self-administration tests to examine the effects of capsazepine (CPZ) and SB366791 (SB) on MAP reward. We found that both CPZ and SB significantly inhibited MAP-induced CPP and self-administration; in contrast, TRPV1 knock-out (KO) mice did not develop MAP-induced CPP. Real-time RT-PCR, Western blot and quantitative autoradiographic tests showed up-regulation of TRPV1 mRNA and protein expression in the NAc and/or DSt regions of mice exhibiting MAP-induced CPP. In addition, an in vivo microdialysis experiment showed that CPZ dramatically reduced dopamine (DA) levels in the NAc region of MAP-treated mice. Furthermore, attenuated dopamine transporter (DAT) binding levels in the NAc and DSt regions of MAP-induced CPP mice were reversed by CPZ. Together, these data suggest that TRPV1 plays an important role in MAP reward via the modulation of DA release and DAT density, thereby providing a novel therapeutic target for MAP addiction.
Keywords	Medicine ; R ; Science ; Q
Subject code	500
Language	English
Publishing date	2018-01-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
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Article ; Online: Blockade of TRPV1 Inhibits Methamphetamine-induced Rewarding Effects.

Tian, Yu-Hua / Ma, Shi-Xun / Lee, Kwang-Wook / Wee, Sunmee / Koob, George F / Lee, Seok-Yong / Jang, Choon-Gon

Scientific reports

2018 Volume 8, Issue 1, Page(s) 882

Abstract: Methamphetamine (MAP) is the most widely used psychostimulant in the world, but the exact mechanisms underlying MAP addiction are not yet fully understood. Recent studies have identified the distribution of TRPV1 in several brain regions that are related ...

Abstract	Methamphetamine (MAP) is the most widely used psychostimulant in the world, but the exact mechanisms underlying MAP addiction are not yet fully understood. Recent studies have identified the distribution of TRPV1 in several brain regions that are related to drug addiction, including nucleus accumbens (NAc) and dorsal striatum (DSt). In the present study, we performed conditioned place preference (CPP) and self-administration tests to examine the effects of capsazepine (CPZ) and SB366791 (SB) on MAP reward. We found that both CPZ and SB significantly inhibited MAP-induced CPP and self-administration; in contrast, TRPV1 knock-out (KO) mice did not develop MAP-induced CPP. Real-time RT-PCR, Western blot and quantitative autoradiographic tests showed up-regulation of TRPV1 mRNA and protein expression in the NAc and/or DSt regions of mice exhibiting MAP-induced CPP. In addition, an in vivo microdialysis experiment showed that CPZ dramatically reduced dopamine (DA) levels in the NAc region of MAP-treated mice. Furthermore, attenuated dopamine transporter (DAT) binding levels in the NAc and DSt regions of MAP-induced CPP mice were reversed by CPZ. Together, these data suggest that TRPV1 plays an important role in MAP reward via the modulation of DA release and DAT density, thereby providing a novel therapeutic target for MAP addiction.
MeSH term(s)	Animals ; Central Nervous System Stimulants/pharmacology ; Conditioning (Psychology)/physiology ; Conditioning, Classical/physiology ; Dopamine/metabolism ; Dopamine Plasma Membrane Transport Proteins/metabolism ; Female ; Male ; Methamphetamine/pharmacology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nucleus Accumbens/metabolism ; Reward ; Signal Transduction/physiology ; TRPV Cation Channels/antagonists & inhibitors ; TRPV Cation Channels/metabolism
Chemical Substances	Central Nervous System Stimulants ; Dopamine Plasma Membrane Transport Proteins ; TRPV Cation Channels ; TRPV1 protein, mouse ; Methamphetamine (44RAL3456C) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2018-01-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-19207-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Self-administration of mixtures of fenfluramine and amphetamine by rhesus monkeys.

Wee, Sunmee / Woolverton, William L

Pharmacology, biochemistry, and behavior

2006 Volume 84, Issue 2, Page(s) 337–343

Abstract: Previous research with psychostimulants has suggested a negative relationship between both potency and efficacy as a reinforcer and serotonergic potency, particularly relative to dopaminergic potency. The present experiment was designed to examine the ... ...

Abstract	Previous research with psychostimulants has suggested a negative relationship between both potency and efficacy as a reinforcer and serotonergic potency, particularly relative to dopaminergic potency. The present experiment was designed to examine the relationship between the serotonergic activity and efficacy as a reinforcer by allowing rhesus monkeys (n=5) to self-administer amphetamine mixed with a serotonin releaser, fenfluramine. Additionally, the role of 5-HT2 receptors in the interaction between amphetamine and fenfluramine was investigated using ketanserin, a selective 5-HT2 receptor antagonist. Amphetamine and fenfluramine were combined in ratios of, respectively, 1:1 to 1:10 on a mg/kg basis and made available for self-administration under a progressive-ratio schedule of reinforcement. Amphetamine (0.0056-0.1 mg/kg/injection) functioned as a positive reinforcer with sigmoidal or biphasic dose-response functions. The addition of fenfluramine to amphetamine decreased the maximum responding, at least at the highest dose ratio (1:10, amphetamine/fenfluramine), in all monkeys. When measured after the pretreatment of ketanserin (1.0-3.0 mg/kg, i.m.), the self-administration of the mixture of amphetamine and fenfluramine at a ratio of 1:10 decreased in three monkeys and was unaffected in the fourth. These results support the notion of a negative influence of increased serotonergic neurotransmission on reinforcing efficacy of drugs that act via monoamine systems. However, the involvement of 5-HT2 receptors in the interaction between the serotonergic system and the reinforcing efficacy still remains equivocal.
MeSH term(s)	Animals ; Dextroamphetamine/administration & dosage ; Fenfluramine/administration & dosage ; Ketanserin/pharmacology ; Macaca mulatta ; Male ; Receptors, Serotonin, 5-HT2/drug effects ; Receptors, Serotonin, 5-HT2/physiology ; Self Administration
Chemical Substances	Receptors, Serotonin, 5-HT2 ; Fenfluramine (2DS058H2CF) ; Ketanserin (97F9DE4CT4) ; Dextroamphetamine (TZ47U051FI)
Language	English
Publishing date	2006-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	191042-5
ISSN	1873-5177 ; 0091-3057
ISSN (online)	1873-5177
ISSN	0091-3057
DOI	10.1016/j.pbb.2006.05.022
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Article ; Online: Regulator of G-Protein Signaling 7 Regulates Reward Behavior by Controlling Opioid Signaling in the Striatum.

Sutton, Laurie P / Ostrovskaya, Olga / Dao, Maria / Xie, Keqiang / Orlandi, Cesare / Smith, Roy / Wee, Sunmee / Martemyanov, Kirill A

Biological psychiatry

2016 Volume 80, Issue 3, Page(s) 235–245

Abstract: Background: Morphine mediates its euphoric and analgesic effects by acting on the μ-opioid receptor (MOR). MOR belongs to the family of G-protein coupled receptors whose signaling efficiency is controlled by the regulator of G-protein signaling (RGS) ... ...

Abstract	Background: Morphine mediates its euphoric and analgesic effects by acting on the μ-opioid receptor (MOR). MOR belongs to the family of G-protein coupled receptors whose signaling efficiency is controlled by the regulator of G-protein signaling (RGS) proteins. Our understanding of the molecular diversity of RGS proteins that control MOR signaling, their circuit specific actions, and underlying cellular mechanisms is very limited. Methods: We used genetic approaches to ablate regulator of G-protein signaling 7 (RGS7) both globally and in specific neuronal populations. We used conditioned place preference and self-administration paradigms to examine reward-related behavior and a battery of tests to assess analgesia, tolerance, and physical dependence to morphine. Electrophysiology approaches were applied to investigate the impact of RGS7 on morphine-induced alterations in neuronal excitability and plasticity of glutamatergic synapses. At least three animals were used for each assessment. Results: Elimination of RGS7 enhanced reward, increased analgesia, delayed tolerance, and heightened withdrawal in response to morphine administration. RGS7 in striatal neurons was selectively responsible for determining the sensitivity of rewarding and reinforcing behaviors to morphine without affecting analgesia, tolerance, and withdrawal. In contrast, deletion of RGS7 in dopaminergic neurons did not influence morphine reward. RGS7 exerted its effects by controlling morphine-induced changes in excitability of medium spiny neurons in nucleus accumbens and gating the compositional plasticity of α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid and N-methyl-D-aspartate receptors. Conclusions: This study identifies RGS7 as a novel regulator of MOR signaling by dissecting its circuit specific actions and pinpointing its role in regulating morphine reward by controlling the activity of nucleus accumbens neurons.
MeSH term(s)	Animals ; Conditioning (Psychology) ; Corpus Striatum/drug effects ; Corpus Striatum/metabolism ; Corpus Striatum/physiology ; Dopaminergic Neurons/metabolism ; Dopaminergic Neurons/physiology ; Drug Tolerance/physiology ; Female ; Glutamic Acid/physiology ; Male ; Mice ; Mice, Knockout ; Morphine/pharmacology ; Neurons/physiology ; Nucleus Accumbens/physiology ; Pain Measurement/drug effects ; RGS Proteins/genetics ; RGS Proteins/metabolism ; RGS Proteins/physiology ; Reward ; Self Administration ; Signal Transduction/drug effects ; Substance Withdrawal Syndrome/physiopathology
Chemical Substances	RGS Proteins ; Rgs6 protein, mouse ; Rgs7 protein, mouse ; Glutamic Acid (3KX376GY7L) ; Morphine (76I7G6D29C)
Language	English
Publishing date	2016-08-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2015.07.026
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Article: Evaluation of the reinforcing effects of atomoxetine in monkeys: comparison to methylphenidate and desipramine.

Wee, Sunmee / Woolverton, William L

Drug and alcohol dependence

2004 Volume 75, Issue 3, Page(s) 271–276

Abstract: Atomoxetine is a selective norepinephrine (NE) reuptake blocker that has recently been marketed for the treatment of attention deficit hyperactivity disorder. The purpose of the present study was to evaluate the self-administration of atomoxetine in an ... ...

Abstract	Atomoxetine is a selective norepinephrine (NE) reuptake blocker that has recently been marketed for the treatment of attention deficit hyperactivity disorder. The purpose of the present study was to evaluate the self-administration of atomoxetine in an animal model predictive of abuse liability in humans. Rhesus monkeys (N = 5) were prepared with chronic intravenous catheters and allowed to self-administer cocaine or saline during alternating baseline sessions. When behavior was stable, atomoxetine (0.03-3.0 mg/kg per injection), desipramine (0.1-3.0 mg/kg per injection), methylphenidate (0.001-0.1 mg/kg per injection), or their vehicles were substituted for baseline conditions. Methylphenidate consistently maintained responding above the levels maintained by its vehicle. Atomoxetine and desipramine failed to reliably maintain self-administration above vehicle levels in four of five individual monkeys. These results predict that atomoxetine, in contrast to methylphenidate but like desipramine, will lack reinforcing effects and abuse potential in humans.
MeSH term(s)	Animals ; Atomoxetine Hydrochloride ; Desipramine/pharmacology ; Dose-Response Relationship, Drug ; Drug Evaluation, Preclinical/methods ; Macaca mulatta ; Male ; Methylphenidate/pharmacology ; Propylamines/pharmacology ; Reaction Time/drug effects ; Reaction Time/physiology ; Reinforcement (Psychology) ; Self Administration
Chemical Substances	Propylamines ; Methylphenidate (207ZZ9QZ49) ; Atomoxetine Hydrochloride (57WVB6I2W0) ; Desipramine (TG537D343B)
Language	English
Publishing date	2004-09-06
Publishing country	Ireland
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	519918-9
ISSN	1879-0046 ; 0376-8716
ISSN (online)	1879-0046
ISSN	0376-8716
DOI	10.1016/j.drugalcdep.2004.03.010
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Article ; Online: A combination of buprenorphine and naltrexone blocks compulsive cocaine intake in rodents without producing dependence.

Wee, Sunmee / Vendruscolo, Leandro F / Misra, Kaushik K / Schlosburg, Joel E / Koob, George F

Science translational medicine

2012 Volume 4, Issue 146, Page(s) 146ra110

Abstract: Buprenorphine, a synthetic opioid that acts at both μ and κ opioid receptors, can decrease cocaine use in individuals with opioid addiction. However, the potent agonist action of buprenorphine at μ opioid receptors raises its potential for creating ... ...

Abstract	Buprenorphine, a synthetic opioid that acts at both μ and κ opioid receptors, can decrease cocaine use in individuals with opioid addiction. However, the potent agonist action of buprenorphine at μ opioid receptors raises its potential for creating opioid dependence in non-opioid-dependent cocaine abusers. Here, we tested the hypothesis that a combination of buprenorphine and naltrexone (a potent μ opioid antagonist with weaker δ and κ antagonist properties) could block compulsive cocaine self-administration without producing opioid dependence. The effects of buprenorphine and various doses of naltrexone on cocaine self-administration were assessed in rats that self-administered cocaine under conditions of either short access (noncompulsive cocaine seeking) or extended access (compulsive cocaine seeking). Buprenorphine alone reproducibly decreased cocaine self-administration. Although this buprenorphine-alone effect was blocked in a dose-dependent manner by naltrexone in both the short-access and the extended-access groups, the combination of the lowest dose of naltrexone with buprenorphine blocked cocaine self-administration in the extended-access group but not in the short-access group. Rats given this low dose of naltrexone with buprenorphine did not exhibit the physical opioid withdrawal syndrome seen in rats treated with buprenorphine alone, and naltrexone at this dose did not block κ agonist-induced analgesia. The results suggest that the combination of buprenorphine and naltrexone at an appropriate dosage decreases compulsive cocaine self-administration with minimal liability to produce opioid dependence and may be useful as a treatment for cocaine addiction.
MeSH term(s)	Animals ; Buprenorphine/therapeutic use ; Cocaine/adverse effects ; Cocaine-Related Disorders/drug therapy ; Cocaine-Related Disorders/prevention & control ; Male ; Naloxone/adverse effects ; Naltrexone/therapeutic use ; Rats ; Rats, Wistar ; Substance Withdrawal Syndrome/prevention & control
Chemical Substances	Naloxone (36B82AMQ7N) ; Buprenorphine (40D3SCR4GZ) ; Naltrexone (5S6W795CQM) ; Cocaine (I5Y540LHVR)
Language	English
Publishing date	2012-08-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.3003948
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Article: Effects of dose and session duration on cocaine self-administration in rats.

Wee, Sunmee / Specio, Sheila E / Koob, George F

The Journal of pharmacology and experimental therapeutics

2007 Volume 320, Issue 3, Page(s) 1134–1143

Abstract: Previous studies showed that an extended 6-h session duration produced an increasing rate of cocaine self-administration in rats. The present study further investigated the effect of dose and session duration on cocaine self-administration. Eight groups ... ...

Abstract	Previous studies showed that an extended 6-h session duration produced an increasing rate of cocaine self-administration in rats. The present study further investigated the effect of dose and session duration on cocaine self-administration. Eight groups of rats (4 doses x 2 session durations) self-administered one of four cocaine doses (0.25, 0.5, 1, and 2 mg/kg/injection) in either 1- or 6-h sessions under a fixed-ratio schedule. In another experiment, two other groups of rats self-administered 0.5 mg/kg/injection of cocaine in either 3- or 12-h sessions. Cocaine self-administration increased at all doses in 6-h sessions but not in 1-h sessions. Cocaine intake (milligram/kilogram) reached an asymptote earlier at a higher dose, but the rate of responding increased faster when the dose was lower. In ShA rats, the cocaine dose-response function was higher in rats at the two higher unit doses than at the lower doses. Cocaine self-administration increased in 6- and 12-h sessions, but not in 1- and 3-h sessions. The increase in self-administration was faster and greater in 12-h sessions than 6-h sessions. The data suggest that cocaine self-administration increases at various doses with prolonged access and that an increase in the rate of responding is positively and inversely associated with session duration and unit dose, respectively. Results also imply that cocaine intake reaches a ceiling faster at high doses even under short session duration. Therefore, high doses or prolonged access to cocaine are more likely to result in a pattern of cocaine intake that reflects compulsive use.
MeSH term(s)	Animals ; Cocaine/administration & dosage ; Dose-Response Relationship, Drug ; Injections, Intravenous ; Male ; Rats ; Rats, Wistar ; Self Administration ; Time Factors
Chemical Substances	Cocaine (I5Y540LHVR)
Language	English
Publishing date	2007-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
DOI	10.1124/jpet.106.113340
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Article ; Online: A dysphoric-like state during early withdrawal from extended access to methamphetamine self-administration in rats.

Jang, Choon-Gon / Whitfield, Timothy / Schulteis, Gery / Koob, George F / Wee, Sunmee

Psychopharmacology

2012 Volume 225, Issue 3, Page(s) 753–763

Abstract: Rationale: Negative emotional states during drug withdrawal may contribute to compulsive drug intake and seeking in humans. Studies suggest that extended access to methamphetamine induces compulsive drug intake in rats.: Objective: The present study ... ...

Abstract	Rationale: Negative emotional states during drug withdrawal may contribute to compulsive drug intake and seeking in humans. Studies suggest that extended access to methamphetamine induces compulsive drug intake in rats. Objective: The present study tested the hypothesis that compulsive methamphetamine intake in rats with extended access is associated with negative emotional states during drug withdrawal. Methods: Rats with short (1 h, ShA) and extended access (6 h, LgA) to methamphetamine self-administration (0.05 mg/kg/infusion) were tested for reward thresholds using intracranial self-stimulation (ICSS). Different groups of ShA and LgA rats were examined for depression-like and anxiety-like states in the novelty-suppressed feeding, open field, defensive burying, and forced swim tests. Results: With extended access, ICSS thresholds gradually increased, which was correlated with the increase of drug intake. During drug withdrawal, the increased ICSS thresholds returned to levels observed before exposure to extended access to methamphetamine. Upon re-exposure to extended access to methamphetamine, ICSS thresholds showed a more rapid escalation than during the initial exposure. LgA rats showed a longer latency to approach chow in the center of a novel field and remained immobile longer in the forced swim test than ShA rats did during early withdrawal. In contrast, ShA rats actively buried an aversive shock probe whereas LgA rats remained immobile in the defensive burying test. Conclusion: The data suggest that extended access to methamphetamine produces a more depressive-like state than anxiety-like state in rats during early withdrawal.
MeSH term(s)	Animals ; Compulsive Behavior/psychology ; Dose-Response Relationship, Drug ; Drug-Seeking Behavior/drug effects ; Electric Stimulation ; Emotions/drug effects ; Male ; Methamphetamine/administration & dosage ; Methamphetamine/adverse effects ; Rats ; Rats, Wistar ; Reward ; Self Administration ; Self Stimulation ; Substance Withdrawal Syndrome/psychology ; Time Factors
Chemical Substances	Methamphetamine (44RAL3456C)
Language	English
Publishing date	2012-09-25
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	130601-7
ISSN	1432-2072 ; 0033-3158
ISSN (online)	1432-2072
ISSN	0033-3158
DOI	10.1007/s00213-012-2864-0
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Article ; Online: Self-administration of ethanol, cocaine, or nicotine does not decrease the soma size of ventral tegmental area dopamine neurons.

Mazei-Robison, Michelle S / Appasani, Raghu / Edwards, Scott / Wee, Sunmee / Taylor, Seth R / Picciotto, Marina R / Koob, George F / Nestler, Eric J

PloS one

2014 Volume 9, Issue 4, Page(s) e95962

Abstract: Our previous observations show that chronic opiate administration, including self-administration, decrease the soma size of dopamine (DA) neurons in the ventral tegmental area (VTA) of rodents and humans, a morphological change correlated with increased ... ...

Abstract	Our previous observations show that chronic opiate administration, including self-administration, decrease the soma size of dopamine (DA) neurons in the ventral tegmental area (VTA) of rodents and humans, a morphological change correlated with increased firing rate and reward tolerance. Given that a general hallmark of drugs of abuse is to increase activity of the mesolimbic DA circuit, we sought to determine whether additional drug classes produced a similar morphological change. Sections containing VTA were obtained from rats that self-administered cocaine or ethanol and from mice that consumed nicotine. In contrast to opiates, we found no change in VTA DA soma size induced by any of these other drugs. These data suggest that VTA morphological changes are induced in a drug-specific manner and reinforce recent findings that some changes in mesolimbic signaling and neuroplasticity are drug-class dependent.
MeSH term(s)	Animals ; Cell Size/drug effects ; Cocaine/pharmacology ; Dopaminergic Neurons/drug effects ; Dopaminergic Neurons/physiology ; Ethanol/pharmacology ; Male ; Mice, Inbred C57BL ; Nicotine/pharmacology ; Rats, Wistar ; Self Administration ; Ventral Tegmental Area/cytology ; Ventral Tegmental Area/drug effects
Chemical Substances	Ethanol (3K9958V90M) ; Nicotine (6M3C89ZY6R) ; Cocaine (I5Y540LHVR)
Language	English
Publishing date	2014-04-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0095962
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