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  1 / 18646 MEDLINE  
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PMID:28466068
Autor:McMurray MS; Conway SM; Roitman JD
Endereço:Department of Psychology, Miami University, Oxford, OH 45056.
Título:Brain Stimulation Reward Supports More Consistent and Accurate Rodent Decision-Making than Food Reward.
Fonte:eNeuro; 4(2), 2017 Mar-Apr.
ISSN:2373-2822
País de publicação:United States
Idioma:eng
Resumo:Animal models of decision-making rely on an animal's motivation to decide and its ability to detect differences among various alternatives. Food reinforcement, although commonly used, is associated with problematic confounds, especially satiety. Here, we examined the use of brain stimulation reward (BSR) as an alternative reinforcer in rodent models of decision-making and compared it with the effectiveness of sugar pellets. The discriminability of various BSR frequencies was compared to differing numbers of sugar pellets in separate free-choice tasks. We found that BSR was more discriminable and motivated greater task engagement and more consistent preference for the larger reward. We then investigated whether rats prefer BSR of varying frequencies over sugar pellets. We found that animals showed either a clear preference for sugar reward or no preference between reward modalities, depending on the frequency of the BSR alternative and the size of the sugar reward. Overall, these results suggest that BSR is an effective reinforcer in rodent decision-making tasks, removing food-related confounds and resulting in more accurate, consistent, and reliable metrics of choice.
Tipo de publicação: JOURNAL ARTICLE


  2 / 18646 MEDLINE  
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PMID:29335427
Autor:Renteria R; Baltz ET; Gremel CM
Endereço:Department of Psychology, University of California San Diego, La Jolla, CA, 92093, USA.
Título:Chronic alcohol exposure disrupts top-down control over basal ganglia action selection to produce habits.
Fonte:Nat Commun; 9(1):211, 2018 01 15.
ISSN:2041-1723
País de publicação:England
Idioma:eng
Resumo:Addiction involves a predominance of habitual control mediated through action selection processes in dorsal striatum. Research has largely focused on neural mechanisms mediating a proposed progression from ventral to dorsal lateral striatal control in addiction. However, over reliance on habit striatal processes may also arise from reduced cortical input to striatum, thereby disrupting executive control over action selection. Here, we identify novel mechanisms through which chronic intermittent ethanol exposure and withdrawal (CIE) disrupts top-down control over goal-directed action selection processes to produce habits. We find CIE results in decreased excitability of orbital frontal cortex (OFC) excitatory circuits supporting goal-directed control, and, strikingly, selectively reduces OFC output to the direct output pathway in dorsal medial striatum. Increasing the activity of OFC circuits restores goal-directed control in CIE-exposed mice. Our findings show habitual control in alcohol dependence can arise through disrupted communication between top-down, goal-directed processes onto basal ganglia pathways controlling action selection.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Central Nervous System Depressants); 3K9958V90M (Ethanol)


  3 / 18646 MEDLINE  
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PMID:28743727
Autor:Lichtenberg NT; Pennington ZT; Holley SM; Greenfield VY; Cepeda C; Levine MS; Wassum KM
Endereço:Department of Psychology and.
Título:Basolateral Amygdala to Orbitofrontal Cortex Projections Enable Cue-Triggered Reward Expectations.
Fonte:J Neurosci; 37(35):8374-8384, 2017 Aug 30.
ISSN:1529-2401
País de publicação:United States
Idioma:eng
Resumo:To make an appropriate decision, one must anticipate potential future rewarding events, even when they are not readily observable. These expectations are generated by using observable information (e.g., stimuli or available actions) to retrieve often quite detailed memories of available rewards. The basolateral amygdala (BLA) and orbitofrontal cortex (OFC) are two reciprocally connected key nodes in the circuitry supporting such outcome-guided behaviors. But there is much unknown about the contribution of this circuit to decision making, and almost nothing known about the whether any contribution is via direct, monosynaptic projections, or the direction of information transfer. Therefore, here we used designer receptor-mediated inactivation of OFC→BLA or BLA→OFC projections to evaluate their respective contributions to outcome-guided behaviors in rats. Inactivation of BLA terminals in the OFC, but not OFC terminals in the BLA, disrupted the selective motivating influence of cue-triggered reward representations over reward-seeking decisions as assayed by Pavlovian-to-instrumental transfer. BLA→OFC projections were also required when a cued reward representation was used to modify Pavlovian conditional goal-approach responses according to the reward's current value. These projections were not necessary when actions were guided by reward expectations generated based on learned action-reward contingencies, or when rewards themselves, rather than stored memories, directed action. These data demonstrate that BLA→OFC projections enable the cue-triggered reward expectations that can motivate the execution of specific action plans and allow adaptive conditional responding. Deficits anticipating potential future rewarding events are associated with many psychiatric diseases. Presently, we know little about the neural circuits supporting such reward expectation. Here we show that basolateral amygdala to orbitofrontal cortex projections are required for expectations of specific available rewards to influence reward seeking and decision making. The necessity of these projections was limited to situations in which expectations were elicited by reward-predictive cues. These projections therefore facilitate adaptive behavior by enabling the orbitofrontal cortex to use environmental stimuli to generate expectations of potential future rewarding events.
Tipo de publicação: JOURNAL ARTICLE


  4 / 18646 MEDLINE  
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PMID:28451642
Autor:Moschak TM; Carelli RM
Endereço:Department of Psychology and Neuroscience, University of North Carolina, Chapel Hill, NC 27599.
Título:Impulsive Rats Exhibit Blunted Dopamine Release Dynamics during a Delay Discounting Task Independent of Cocaine History.
Fonte:eNeuro; 4(2), 2017 Mar-Apr.
ISSN:2373-2822
País de publicação:United States
Idioma:eng
Resumo:The inability to wait for a large, delayed reward when faced with a small, immediate one, known as delay discounting, has been implicated in a number of disorders including substance abuse. Individual differences in impulsivity on the delay discounting task are reflected in differences in neural function, including in the nucleus accumbens (NAc) core. We examined the role of a history of cocaine self-administration, as well as individual differences in impulsivity, on rapid dopamine (DA) release dynamics in the NAc core. Rats with a history of cocaine or water/saline self-administration were tested on delay discounting while being simultaneously assayed for rapid DA release using electrochemical methods. In controls, we found that cue DA release was modulated by reward delay and magnitude, consistent with prior reports. A history of cocaine had no effect on either delay discounting or DA release dynamics. Nonetheless, independent of drug history, individual differences in impulsivity were related to DA release in the NAc core. First, high impulsive animals exhibited dampened cue DA release during the delay discounting task. Second, reward delay and magnitude in high impulsive animals failed to robustly modulate changes in cue DA release. Importantly, these two DAergic mechanisms were uncorrelated with each other and, together, accounted for a high degree of variance in impulsive behavior. Collectively, these findings demonstrate two distinct mechanisms by which rapid DA signaling may influence impulsivity, and illustrate the importance of NAc core DA release dynamics in impulsive behavior.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
Nome de substância:I5Y540LHVR (Cocaine); VTD58H1Z2X (Dopamine)


  5 / 18646 MEDLINE  
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PMID:28451632
Autor:Galvão-Ferreira P; Lipinski M; Santos F; Barco A; Costa RM
Endereço:Champalimaud Neuroscience Programme, Fundação Champalimaud, Lisbon, 1400-038 Portugal.
Título:Skill Learning Modulates RNA Pol II Poising at Immediate Early Genes in the Adult Striatum.
Fonte:eNeuro; 4(2), 2017 Mar-Apr.
ISSN:2373-2822
País de publicação:United States
Idioma:eng
Resumo:A multilayered complexity of epigenetic and transcriptional regulatory mechanisms underlies neuronal activity-dependent gene transcription. The regulation of RNA Pol II progression along the transcription cycle, from promoter-proximal poising (with RNA Pol II paused at promoter-proximal regions, characterized by a Ser5P -rich and Ser2P -poor RPB1 CTD) to active elongation, has emerged as a major step in transcriptional regulation across several organisms, tissues, and developmental stages, including the nervous system. However, it is not known whether this mechanism is modulated by experience. We investigated the impact of learning a motor skill on RNA Pol II phosphorylation dynamics in the adult mouse striatum. We uncovered that learning modulates the striatal phosphorylation dynamics of the CTD of the RNA Pol II RPB1 subunit, leading to an increased poising index in trained mice. We found that this modulation occurs at immediate early genes (IEGs), with increased poising of RNA Pol II at both and genes but not at constitutively expressed genes. Furthermore, we confirmed that this was learning dependent, and not just regulated by context or motor activity. These experiments demonstrate a novel phenomenon of learning induced transcriptional modulation in adult brain, which may have implications for our understanding of learning, memory allocation, and consolidation.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:EC 2.7.7.- (RNA Polymerase II); EC 2.7.7.- (Rpb1 protein, mouse)


  6 / 18646 MEDLINE  
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PMID:29251972
Autor:Hutsell BA; Banks ML
Endereço:Department of Pharmacology and Toxicology, Virginia Commonwealth University.
Título:Remifentanil maintains lower initial delayed nonmatching-to-sample accuracy compared to food pellets in male rhesus monkeys.
Fonte:Exp Clin Psychopharmacol; 25(6):441-447, 2017 12.
ISSN:1936-2293
País de publicação:United States
Idioma:eng
Resumo:Emerging human laboratory and preclinical drug self-administration data suggest that a history of contingent abused drug exposure impairs performance in operant discrimination procedures, such as delayed nonmatching-to-sample (DNMTS), that are hypothesized to assess components of executive function. However, these preclinical discrimination studies have exclusively used food as the reinforcer and the effects of drugs as reinforcers in these operant procedures are unknown. The present study determined effects of contingent intravenous remifentanil injections on DNMTS performance hypothesized to assess 1 aspect of executive function, working memory. Daily behavioral sessions consisted of 2 components with sequential intravenous remifentanil (0, 0.01-1.0 µg/kg/injection) or food (0, 1-10 pellets) availability in nonopioid dependent male rhesus monkeys (n = 3). Remifentanil functioned as a reinforcer in the DNMTS procedure. Similar delay-dependent DNMTS accuracy was observed under both remifentanil- and food-maintained components, such that higher accuracies were maintained at shorter (0.1-1.0 s) delays and lower accuracies approaching chance performance were maintained at longer (10-32 s) delays. Remifentanil maintained significantly lower initial DNMTS accuracy compared to food. Reinforcer magnitude was not an important determinant of DNMTS accuracy for either remifentanil or food. These results extend the range of experimental procedures under which drugs function as reinforcers. Furthermore, the selective remifentanil-induced decrease in initial DNMTS accuracy is consistent with a selective impairment of attentional, but not memorial, processes. (PsycINFO Database Record
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
Nome de substância:0 (Anesthetics, Intravenous); 0 (Piperidines); P10582JYYK (remifentanil)


  7 / 18646 MEDLINE  
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PMID:28449946
Autor:Thrailkill EA; Bouton ME
Endereço:University of Vermont, United States. Electronic address: eric.thrailkill@uvm.edu.
Título:Factors that influence the persistence and relapse of discriminated behavior chains.
Fonte:Behav Processes; 141(Pt 1):3-10, 2017 Aug.
ISSN:1872-8308
País de publicação:Netherlands
Idioma:eng
Resumo:Behavior chains are composed of sequences of behaviors that minimally include procurement and then consumption. This review surveys recent research from this laboratory that has examined the properties of discriminated heterogeneous behavior chains. In contrast to another review (Thrailkill and Bouton, 2016a), it discusses work examining what makes chained behavior persistent, and what makes it relapse. Results suggest that responses in a discriminated heterogeneous behavior chain may become associated, so that extinction of either one reduces the strength of the other. Evidence also suggests that the goal of the first (procurement) response may be the next (consumption) response (rather than the upcoming discriminative stimulus, a putative conditioned reinforcer, or the primary reinforcer at the end of the chain). Further studies suggest that methods that promote generalization across acquisition and extinction (partial reinforcement and delivery of noncontingent reinforcers during extinction) lead to greater persistence of the procurement response. A third set of studies analyzed the contextual control and relapse of chained behaviors. The context controls both the acquisition and extinction of chained behaviors. In addition, a separately-extinguished consumption response is renewed when returned to the context of the chain. The research expands our general understanding of the learning processes that govern instrumental behavior as well as our understanding of chains.
Tipo de publicação: JOURNAL ARTICLE; REVIEW


  8 / 18646 MEDLINE  
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PMID:29184209
Autor:Rodriguez E; Sakurai K; Xu J; Chen Y; Toda K; Zhao S; Han BX; Ryu D; Yin H; Liedtke W; Wang F
Endereço:Department of Neurobiology, Duke University Medical Center, Durham, NC, USA.
Título:A craniofacial-specific monosynaptic circuit enables heightened affective pain.
Fonte:Nat Neurosci; 20(12):1734-1743, 2017 Dec.
ISSN:1546-1726
País de publicação:United States
Idioma:eng
Resumo:Humans often rank craniofacial pain as more severe than body pain. Evidence suggests that a stimulus of the same intensity induces stronger pain in the face than in the body. However, the underlying neural circuitry for the differential processing of facial versus bodily pain remains unknown. Interestingly, the lateral parabrachial nucleus (PB ), a critical node in the affective pain circuit, is activated more strongly by noxious stimulation of the face than of the hindpaw. Using a novel activity-dependent technology called CANE developed in our laboratory, we identified and selectively labeled noxious-stimulus-activated PB neurons and performed comprehensive anatomical input-output mapping. Surprisingly, we uncovered a hitherto uncharacterized monosynaptic connection between cranial sensory neurons and the PB -nociceptive neurons. Optogenetic activation of this monosynaptic craniofacial-to-PB projection induced robust escape and avoidance behaviors and stress calls, whereas optogenetic silencing specifically reduced facial nociception. The monosynaptic circuit revealed here provides a neural substrate for heightened craniofacial affective pain.
Tipo de publicação: JOURNAL ARTICLE


  9 / 18646 MEDLINE  
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PMID:29339724
Autor:Calipari ES; Godino A; Peck EG; Salery M; Mervosh NL; Landry JA; Russo SJ; Hurd YL; Nestler EJ; Kiraly DD
Endereço:Fishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Título:Granulocyte-colony stimulating factor controls neural and behavioral plasticity in response to cocaine.
Fonte:Nat Commun; 9(1):9, 2018 01 16.
ISSN:2041-1723
País de publicação:England
Idioma:eng
Resumo:Cocaine addiction is characterized by dysfunction in reward-related brain circuits, leading to maladaptive motivation to seek and take the drug. There are currently no clinically available pharmacotherapies to treat cocaine addiction. Through a broad screen of innate immune mediators, we identify granulocyte-colony stimulating factor (G-CSF) as a potent mediator of cocaine-induced adaptations. Here we report that G-CSF potentiates cocaine-induced increases in neural activity in the nucleus accumbens (NAc) and prefrontal cortex. In addition, G-CSF injections potentiate cocaine place preference and enhance motivation to self-administer cocaine, while not affecting responses to natural rewards. Infusion of G-CSF neutralizing antibody into NAc blocks the ability of G-CSF to modulate cocaine's behavioral effects, providing a direct link between central G-CSF action in NAc and cocaine reward. These results demonstrate that manipulating G-CSF is sufficient to alter the motivation for cocaine, but not natural rewards, providing a pharmacotherapeutic avenue to manipulate addictive behaviors without abuse potential.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:143011-72-7 (Granulocyte Colony-Stimulating Factor); I5Y540LHVR (Cocaine)


  10 / 18646 MEDLINE  
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PMID:29037662
Autor:Ward M; Norman H; D'Souza MS
Endereço:Department of Pharmaceutical and Biomedical Sciences, The Raabe College of Pharmacy, Ohio Northern University, 525 S Main Street, Ada, OH 45810, United States.
Título:Effects of pharmacological manipulation of the kappa opioid receptors on the aversive effects of nicotine.
Fonte:Behav Brain Res; 338:56-65, 2018 Feb 15.
ISSN:1872-7549
País de publicação:Netherlands
Idioma:eng
Resumo:Nicotine, an addictive component of tobacco smoke, produces both rewarding and aversive effects. Increasing the aversive effects of nicotine may help in promoting smoking cessation. However, neural targets mediating the aversive effects of nicotine have not been fully identified. In this study, we evaluated the role of kappa opioid receptors (KORs) in the aversive effects of nicotine (0.4 mg/kg, base; s.c.) using the nicotine-induced conditioned taste aversion (CTA) model in Wistar rats. The KORs were activated using the selective KOR agonist (±)U-50,488H (0, 0.03, 0.15 & 0.3mg/kg; s.c.) and inhibited using the KOR antagonist nor-binaltorphimine (nor-BNI; 0, 15 & 30mg/kg; s.c.) in separate groups of rats using a between-subjects design. Pretreatment with the KOR agonist (±)U-50,488H (0.3mg/kg) significantly increased aversion for the nicotine-associated solution. Additionally, (±)U-50,488H (0.3mg/kg) on its own induced aversion to the flavored solution associated with it even in the absence of nicotine, suggesting that the KOR agonist induced increase in nicotine-induced aversion was an additive effect. Interestingly, administration of the KOR antagonist nor-BNI (30mg/kg) prior to conditioning with nicotine/saline, but not after conditioning with nicotine/saline, attenuated nicotine-induced aversive effects compared to saline controls. Taken together, these data suggest a role for KORs in the aversive effects of nicotine.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Narcotic Antagonists); 0 (Receptors, Opioid, kappa); 36OOQ86QM1 (norbinaltorphimine); 5S6W795CQM (Naltrexone); 67198-13-4 (3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer); 6M3C89ZY6R (Nicotine)



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