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	<title>CiteULike: Tag nucleus_accumbens</title>
	<description>CiteULike: Tag nucleus_accumbens</description>


	<link>http://www.citeulike.org/tag/nucleus_accumbens</link>
	<dc:publisher>CiteULike.org</dc:publisher>
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        <rdf:li rdf:resource="http://www.citeulike.org/user/psique/article/1220169"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/psique/article/1208474"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/psique/article/2571655"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/psique/article/2423506"/>
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        <rdf:li rdf:resource="http://www.citeulike.org/user/oamg/article/1026530"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/oamg/article/1355835"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/ntvandehey/article/1550623"/>
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<item rdf:about="http://www.citeulike.org/user/psique/article/1860002">
    <title>Molecular Adaptations Underlying Susceptibility and Resistance to Social Defeat in Brain Reward Regions</title>
    <link>http://www.citeulike.org/user/psique/article/1860002</link>
    <description>&lt;i&gt;Cell, Vol. 131, No. 2. (19 October 2007), pp. 391-404.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Summary While stressful life events are an important cause of psychopathology, most individuals exposed to adversity maintain normal psychological functioning. The molecular mechanisms underlying such resilience are poorly understood. Here, we demonstrate that an inbred population of mice subjected to social defeat can be separated into susceptible and unsusceptible subpopulations that differ along several behavioral and physiological domains. By a combination of molecular and electrophysiological techniques, we identify signature adaptations within the mesolimbic dopamine circuit that are uniquely associated with vulnerability or insusceptibility. We show that molecular recapitulations of three prototypical adaptations associated with the unsusceptible phenotype are each sufficient to promote resistant behavior. Our results validate a multidisciplinary approach to examine the neurobiological mechanisms of variations in stress resistance, and illustrate the importance of plasticity within the brain's reward circuits in actively maintaining an emotional homeostasis.</description>
    <dc:title>Molecular Adaptations Underlying Susceptibility and Resistance to Social Defeat in Brain Reward Regions</dc:title>

    <dc:creator>Vaishnav Krishnan</dc:creator>
    <dc:creator>Ming-Hu Han</dc:creator>
    <dc:creator>Danielle Graham</dc:creator>
    <dc:creator>Olivier Berton</dc:creator>
    <dc:creator>William Renthal</dc:creator>
    <dc:creator>Scott Russo</dc:creator>
    <dc:creator>Quincey Laplant</dc:creator>
    <dc:creator>Ami Graham</dc:creator>
    <dc:creator>Michael Lutter</dc:creator>
    <dc:creator>Diane Lagace</dc:creator>
    <dc:creator>Subroto Ghose</dc:creator>
    <dc:creator>Robin Reister</dc:creator>
    <dc:creator>Paul Tannous</dc:creator>
    <dc:creator>Thomas Green</dc:creator>
    <dc:creator>Rachael Neve</dc:creator>
    <dc:creator>Sumana Chakravarty</dc:creator>
    <dc:creator>Arvind Kumar</dc:creator>
    <dc:creator>Amelia Eisch</dc:creator>
    <dc:creator>David Self</dc:creator>
    <dc:creator>Francis Lee</dc:creator>
    <dc:creator>Carol Tamminga</dc:creator>
    <dc:creator>Donald Cooper</dc:creator>
    <dc:creator>Howard Gershenfeld</dc:creator>
    <dc:creator>Eric Nestler</dc:creator>
    <dc:identifier>doi:10.1016/j.cell.2007.09.018</dc:identifier>
    <dc:source>Cell, Vol. 131, No. 2. (19 October 2007), pp. 391-404.</dc:source>
    <dc:date>2007-11-03T12:04:58-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Cell</prism:publicationName>
    <prism:volume>131</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>391</prism:startingPage>
    <prism:endingPage>404</prism:endingPage>
    <prism:category>2007</prism:category>
    <prism:category>depression</prism:category>
    <prism:category>neurotrophic</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>reward</prism:category>
    <prism:category>stress</prism:category>
    <prism:category>vta</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/psique/article/2626462">
    <title>Differential tonic influence of lateral habenula on prefrontal cortex and nucleus accumbens dopamine release</title>
    <link>http://www.citeulike.org/user/psique/article/2626462</link>
    <description>&lt;i&gt;European Journal of Neuroscience, Vol. 27, No. 7. (April 2008), pp. 1755-1762.&lt;/i&gt;</description>
    <dc:title>Differential tonic influence of lateral habenula on prefrontal cortex and nucleus accumbens dopamine release</dc:title>

    <dc:creator>Lecourtier</dc:creator>
    <dc:creator>Lucas</dc:creator>
    <dc:creator>Defrancesco</dc:creator>
    <dc:creator>Alicia</dc:creator>
    <dc:creator>Moghaddam</dc:creator>
    <dc:creator>Bita</dc:creator>
    <dc:identifier>doi:10.1111/j.1460-9568.2008.06130.x</dc:identifier>
    <dc:source>European Journal of Neuroscience, Vol. 27, No. 7. (April 2008), pp. 1755-1762.</dc:source>
    <dc:date>2008-04-03T15:14:26-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>European Journal of Neuroscience</prism:publicationName>
    <prism:issn>0953-816X</prism:issn>
    <prism:volume>27</prism:volume>
    <prism:number>7</prism:number>
    <prism:startingPage>1755</prism:startingPage>
    <prism:endingPage>1762</prism:endingPage>
    <prism:publisher>Blackwell Publishing</prism:publisher>
    <prism:category>dopamine</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>pfc</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/psique/article/1220169">
    <title>Deep Brain Stimulation to Reward Circuitry Alleviates Anhedonia in Refractory Major Depression</title>
    <link>http://www.citeulike.org/user/psique/article/1220169</link>
    <description>&lt;i&gt;Neuropsychopharmacology, Vol. aop, No. current.&lt;/i&gt;</description>
    <dc:title>Deep Brain Stimulation to Reward Circuitry Alleviates Anhedonia in Refractory Major Depression</dc:title>

    <dc:creator>Thomas Schlaepfer</dc:creator>
    <dc:creator>Michael Cohen</dc:creator>
    <dc:creator>Caroline Frick</dc:creator>
    <dc:creator>Markus Kosel</dc:creator>
    <dc:creator>Daniela Brodesser</dc:creator>
    <dc:creator>Nikolai Axmacher</dc:creator>
    <dc:creator>Alexius Joe</dc:creator>
    <dc:creator>Martina Kreft</dc:creator>
    <dc:creator>Doris Lenartz</dc:creator>
    <dc:creator>Volker Sturm</dc:creator>
    <dc:identifier>doi:10.1038/sj.npp.1301408</dc:identifier>
    <dc:source>Neuropsychopharmacology, Vol. aop, No. current.</dc:source>
    <dc:date>2007-04-11T10:15:27-00:00</dc:date>
    <prism:publicationName>Neuropsychopharmacology</prism:publicationName>
    <prism:issn>0893-133X</prism:issn>
    <prism:volume>aop</prism:volume>
    <prism:number>current</prism:number>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>dbs</prism:category>
    <prism:category>depression</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/psique/article/1208474">
    <title>Endocannabinoid Hedonic Hotspot for Sensory Pleasure: Anandamide in Nucleus Accumbens Shell Enhances ‘Liking’ of a Sweet Reward</title>
    <link>http://www.citeulike.org/user/psique/article/1208474</link>
    <description>&lt;i&gt;Neuropsychopharmacology, Vol. aop, No. current.&lt;/i&gt;</description>
    <dc:title>Endocannabinoid Hedonic Hotspot for Sensory Pleasure: Anandamide in Nucleus Accumbens Shell Enhances ‘Liking’ of a Sweet Reward</dc:title>

    <dc:creator>Stephen Mahler</dc:creator>
    <dc:creator>Kyle Smith</dc:creator>
    <dc:creator>Kent Berridge</dc:creator>
    <dc:identifier>doi:10.1038/sj.npp.1301376</dc:identifier>
    <dc:source>Neuropsychopharmacology, Vol. aop, No. current.</dc:source>
    <dc:date>2007-04-05T10:04:27-00:00</dc:date>
    <prism:publicationName>Neuropsychopharmacology</prism:publicationName>
    <prism:issn>0893-133X</prism:issn>
    <prism:volume>aop</prism:volume>
    <prism:number>current</prism:number>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>cannabinoid</prism:category>
    <prism:category>feeding</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>reward</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/psique/article/2571655">
    <title>D2 dopamine modulation of corticoaccumbens synaptic responses changes during adolescence</title>
    <link>http://www.citeulike.org/user/psique/article/2571655</link>
    <description>&lt;i&gt;European Journal of Neuroscience, Vol. 27, No. 6. (March 2008), pp. 1364-1372.&lt;/i&gt;</description>
    <dc:title>D2 dopamine modulation of corticoaccumbens synaptic responses changes during adolescence</dc:title>

    <dc:creator>Benoit-Marand</dc:creator>
    <dc:creator>Marianne</dc:creator>
    <dc:creator>O'Donnell</dc:creator>
    <dc:creator>Patricio</dc:creator>
    <dc:identifier>doi:10.1111/j.1460-9568.2008.06107.x</dc:identifier>
    <dc:source>European Journal of Neuroscience, Vol. 27, No. 6. (March 2008), pp. 1364-1372.</dc:source>
    <dc:date>2008-03-22T14:21:06-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>European Journal of Neuroscience</prism:publicationName>
    <prism:issn>0953-816X</prism:issn>
    <prism:volume>27</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>1364</prism:startingPage>
    <prism:endingPage>1372</prism:endingPage>
    <prism:publisher>Blackwell Publishing</prism:publisher>
    <prism:category>adolescence</prism:category>
    <prism:category>dopamine</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/psique/article/2423506">
    <title>Synaptic plasticity in the basal ganglia: A similar code for physiological and pathological conditions</title>
    <link>http://www.citeulike.org/user/psique/article/2423506</link>
    <description>&lt;i&gt;Progress in Neurobiology, Vol. In Press, Corrected Proof&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;It is widely accepted that the complexity and adaptability of neuronal communication, which is necessary for integrative and higher functions of the brain, is amply represented by plastic changes occurring at synaptic level. Therefore, long-term modifications of synaptic efficacy between neurons have been considered the cellular basis of learning and memory. Accordingly, there is a plethora of experimental evidence supporting this contention. Indeed, synaptic modifications in the hippocampus, the cerebral and cerebellar cortices regulate composite neuronal functions such those related to cognition, awareness, memory storage, and motion. In recent years, the concept that enduring changes of excitatory glutamatergic synaptic potentials [long-term potentiation (LTP) and long-term depression (LTD)] are not limited to the hippocampus and cortices but occur also in other brain areas has emerged. For instance, plasticity at different excitatory pathways has been clearly demonstrated in the basal ganglia. Here we present an overview of the experimental data regarding synaptic plasticity in the basal ganglia and highlight how results reported in the literature are often contradictory, especially when compared to those obtained in the hippocampal area. In trying to propose possible explanations to some of these contradictions, we present a holistic approach that re-interprets the basal ganglia synaptic plasticity in terms of expression of physiological and pathological phenomena and therapeutic effects of drugs.</description>
    <dc:title>Synaptic plasticity in the basal ganglia: A similar code for physiological and pathological conditions</dc:title>

    <dc:creator>Nicola Berretta</dc:creator>
    <dc:creator>Robert Nistico</dc:creator>
    <dc:creator>Giorgio Bernardi</dc:creator>
    <dc:creator>Nicola Mercuri</dc:creator>
    <dc:identifier>doi:10.1016/j.pneurobio.2007.12.004</dc:identifier>
    <dc:source>Progress in Neurobiology, Vol. In Press, Corrected Proof</dc:source>
    <dc:date>2008-02-24T21:31:18-00:00</dc:date>
    <prism:publicationName>Progress in Neurobiology</prism:publicationName>
    <prism:volume>In Press, Corrected Proof</prism:volume>
    <prism:category>2008</prism:category>
    <prism:category>addiction</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>parkinsons</prism:category>
    <prism:category>plasticity</prism:category>
    <prism:category>striatum</prism:category>
    <prism:category>vta</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/psique/article/1220170">
    <title>Differential Regulation of the Mesoaccumbens Dopamine Circuit by Serotonin2C Receptors in the Ventral Tegmental Area and the Nucleus Accumbens: An In Vivo Microdialysis Study with Cocaine</title>
    <link>http://www.citeulike.org/user/psique/article/1220170</link>
    <description>&lt;i&gt;Neuropsychopharmacology, Vol. aop, No. current.&lt;/i&gt;</description>
    <dc:title>Differential Regulation of the Mesoaccumbens Dopamine Circuit by Serotonin2C Receptors in the Ventral Tegmental Area and the Nucleus Accumbens: An In Vivo Microdialysis Study with Cocaine</dc:title>

    <dc:creator>Sylvia Navailles</dc:creator>
    <dc:creator>Delphine Moison</dc:creator>
    <dc:creator>Kathryn Cunningham</dc:creator>
    <dc:creator>Umberto Spampinato</dc:creator>
    <dc:identifier>doi:10.1038/sj.npp.1301414</dc:identifier>
    <dc:source>Neuropsychopharmacology, Vol. aop, No. current.</dc:source>
    <dc:date>2007-04-11T10:15:27-00:00</dc:date>
    <prism:publicationName>Neuropsychopharmacology</prism:publicationName>
    <prism:issn>0893-133X</prism:issn>
    <prism:volume>aop</prism:volume>
    <prism:number>current</prism:number>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>cocaine</prism:category>
    <prism:category>dopamine</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>serotonin</prism:category>
    <prism:category>vta</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/oamg/article/1026530">
    <title>Neural Predictors of Purchases</title>
    <link>http://www.citeulike.org/user/oamg/article/1026530</link>
    <description>&lt;i&gt;Neuron, Vol. 53, No. 1. (4 January 2007), pp. 147-156.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;SummaryMicroeconomic theory maintains that purchases are driven by a combination of consumer preference and price. Using event-related fMRI, we investigated how people weigh these factors to make purchasing decisions. Consistent with neuroimaging evidence suggesting that distinct circuits anticipate gain and loss, product preference activated the nucleus accumbens (NAcc), while excessive prices activated the insula and deactivated the mesial prefrontal cortex (MPFC) prior to the purchase decision. Activity from each of these regions independently predicted immediately subsequent purchases above and beyond self-report variables. These findings suggest that activation of distinct neural circuits related to anticipatory affect precedes and supports consumers' purchasing decisions.</description>
    <dc:title>Neural Predictors of Purchases</dc:title>

    <dc:creator>Brian Knutson</dc:creator>
    <dc:creator>Scott Rick</dc:creator>
    <dc:creator>Elliott Wimmer</dc:creator>
    <dc:creator>Drazen Prelec</dc:creator>
    <dc:creator>George Loewenstein</dc:creator>
    <dc:identifier>doi:10.1016/j.neuron.2006.11.010</dc:identifier>
    <dc:source>Neuron, Vol. 53, No. 1. (4 January 2007), pp. 147-156.</dc:source>
    <dc:date>2007-01-05T09:42:11-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Neuron</prism:publicationName>
    <prism:volume>53</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>147</prism:startingPage>
    <prism:endingPage>156</prism:endingPage>
    <prism:category>insula</prism:category>
    <prism:category>mesial_prefrontal_cortex</prism:category>
    <prism:category>neuroeconomics</prism:category>
    <prism:category>neuromarketing</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>purchases</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/oamg/article/1355835">
    <title>Ventral-striatal/nucleus-accumbens sensitivity to prediction errors during classification learning.</title>
    <link>http://www.citeulike.org/user/oamg/article/1355835</link>
    <description>&lt;i&gt;Hum Brain Mapp, Vol. 27, No. 4. (April 2006), pp. 306-313.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;A prominent theory in neuroscience suggests reward learning is driven by the discrepancy between a subject's expectation of an outcome and the actual outcome itself. Furthermore, it is postulated that midbrain dopamine neurons relay this mismatch to target regions including the ventral striatum. Using functional MRI (fMRI), we tested striatal responses to prediction errors for probabilistic classification learning with purely cognitive feedback. We used a version of the Rescorla-Wagner model to generate prediction errors for each subject and then entered these in a parametric analysis of fMRI activity. Activation in ventral striatum/nucleus-accumbens (Nacc) increased parametrically with prediction error for negative feedback. This result extends recent neuroimaging findings in reward learning by showing that learning with cognitive feedback also depends on the same circuitry and dopaminergic signaling mechanisms.</description>
    <dc:title>Ventral-striatal/nucleus-accumbens sensitivity to prediction errors during classification learning.</dc:title>

    <dc:creator>PF Rodriguez</dc:creator>
    <dc:creator>AR Aron</dc:creator>
    <dc:creator>RA Poldrack</dc:creator>
    <dc:identifier>doi:10.1002/hbm.20186</dc:identifier>
    <dc:source>Hum Brain Mapp, Vol. 27, No. 4. (April 2006), pp. 306-313.</dc:source>
    <dc:date>2007-06-01T15:45:39-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Hum Brain Mapp</prism:publicationName>
    <prism:issn>1065-9471</prism:issn>
    <prism:volume>27</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>306</prism:startingPage>
    <prism:endingPage>313</prism:endingPage>
    <prism:category>instrumental_conditioning</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>reinforcement_learning</prism:category>
    <prism:category>reward_prediction_error</prism:category>
    <prism:category>ventral_striatum</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/ntvandehey/article/1550623">
    <title>Dopamine and glutamate release in the nucleus accumbens and ventral tegmental area of rat following lateral hypothalamic self-stimulation.</title>
    <link>http://www.citeulike.org/user/ntvandehey/article/1550623</link>
    <description>&lt;i&gt;Neuroscience, Vol. 107, No. 4. (2001), pp. 629-639.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Rewarding hypothalamic brain stimulation is thought to depend on trans-synaptic activation of high-threshold (and thus rarely directly depolarized by rewarding stimulation) dopaminergic fibers of the medial forebrain bundle. We used in vivo microdialysis and high-performance liquid chromatography coupled with electrochemical or fluorometric detection to investigate the concurrent release of dopamine and glutamate in the nucleus accumbens septi and in the ventral tegmental area, as a function of lateral hypothalamic self-stimulation.Self-stimulation at a variety of stimulation frequencies and pulse widths increased levels of dopamine and its primary metabolites, dihydroxyphenylacetic acid and homovanillic acid in the nucleus accumbens. Lateral hypothalamic self-stimulation also induced significant increases in ventral tegmental area dopamine and metabolite levels, and the percentage increase of dopamine was higher in this region than in the nucleus accumbens. Local perfusion with the dopamine uptake inhibitor nomifensine (10 microM) increased dopamine levels in the nucleus accumbens about three-fold and potentiated the increase of dopamine levels induced by self-stimulation. Nomifensine perfusion also induced a delayed decrease in nucleus accumbens glutamate levels, and self-stimulation did not modify this effect of the drug. Local perfusion with the D2-type dopamine receptor antagonist raclopride significantly increased both basal and self-stimulation induced dopamine release in the nucleus accumbens. Neither nomifensine nor raclopride perfusion significantly affected the maximal rates of self-stimulation.Perfusion with tetrodotoxin (2 microM) into nucleus accumbens significantly decreased basal and prevented stimulation-induced increases in accumbens dopamine levels but only slightly decreased the rate of self-stimulation. In contrast, perfusion of tetrodotoxin (0.5 microM) into the ventral tegmental area decreased basal and blocked stimulation-induced increases in both nucleus accumbens and ventral tegmental area dopamine levels; this treatment also blocked or strongly inhibited self-stimulation. While it had no effect on glutamate levels in the nucleus accumbens, lateral hypothalamic self-stimulation induced a significant and tetrodotoxin-sensitive increase in glutamate levels in the ventral tegmental area.Taken together, the present results indicate that, across a broad range of stimulation parameters, rewarding lateral hypothalamus stimulation causes major and persistent activation of the mesolimbic dopamine system, and suggest descending glutamatergic fibers in the medial forebrain bundle as a candidate for the directly activated descending pathway in lateral hypothalamus brain stimulation reward.</description>
    <dc:title>Dopamine and glutamate release in the nucleus accumbens and ventral tegmental area of rat following lateral hypothalamic self-stimulation.</dc:title>

    <dc:creator>ZB You</dc:creator>
    <dc:creator>YQ Chen</dc:creator>
    <dc:creator>RA Wise</dc:creator>
    <dc:source>Neuroscience, Vol. 107, No. 4. (2001), pp. 629-639.</dc:source>
    <dc:date>2007-08-09T21:08:27-00:00</dc:date>
    <prism:publicationYear>2001</prism:publicationYear>
    <prism:publicationName>Neuroscience</prism:publicationName>
    <prism:issn>0306-4522</prism:issn>
    <prism:volume>107</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>629</prism:startingPage>
    <prism:endingPage>639</prism:endingPage>
    <prism:category>dopamine</prism:category>
    <prism:category>glutamate</prism:category>
    <prism:category>hypothalamus</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>stimulation</prism:category>
    <prism:category>ventral_tegmental</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/klouie/article/674659">
    <title>Early consolidation of instrumental learning requires protein synthesis in the nucleus accumbens</title>
    <link>http://www.citeulike.org/user/klouie/article/674659</link>
    <description>&lt;i&gt;Nat Neurosci, Vol. 5, No. 12. (December 2002), pp. 1327-1331.&lt;/i&gt;</description>
    <dc:title>Early consolidation of instrumental learning requires protein synthesis in the nucleus accumbens</dc:title>

    <dc:creator>Pepe Hernandez</dc:creator>
    <dc:creator>Kenneth Sadeghian</dc:creator>
    <dc:creator>Ann Kelley</dc:creator>
    <dc:identifier>doi:10.1038/nn973</dc:identifier>
    <dc:source>Nat Neurosci, Vol. 5, No. 12. (December 2002), pp. 1327-1331.</dc:source>
    <dc:date>2006-05-30T04:03:33-00:00</dc:date>
    <prism:publicationYear>2002</prism:publicationYear>
    <prism:publicationName>Nat Neurosci</prism:publicationName>
    <prism:volume>5</prism:volume>
    <prism:number>12</prism:number>
    <prism:startingPage>1327</prism:startingPage>
    <prism:endingPage>1331</prism:endingPage>
    <prism:category>learning</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>protein_synthesis</prism:category>
    <prism:category>rat</prism:category>
    <prism:category>reward</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/klouie/article/114079">
    <title>Limbic corticostriatal systems and delayed reinforcement.</title>
    <link>http://www.citeulike.org/user/klouie/article/114079</link>
    <description>&lt;i&gt;Ann N Y Acad Sci, Vol. 1021 (June 2004), pp. 33-50.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Impulsive choice, one aspect of impulsivity, is characterized by an abnormally high preference for small, immediate rewards over larger delayed rewards, and can be a feature of adolescence, but also attention-deficit/hyperactivity disorder (ADHD), addiction, and other neuropsychiatric disorders. Both the serotonin and dopamine neuromodulator systems are implicated in impulsivity; manipulations of these systems affect animal models of impulsive choice, though these effects may depend on the receptor subtype and whether or not the reward is signaled. These systems project to limbic cortical and striatal structures shown to be abnormal in animal models of ADHD. Damage to the nucleus accumbens core (AcbC) causes rats to exhibit impulsive choice. These rats are also hyperactive, but are unimpaired in tests of visuospatial attention; they may therefore represent an animal model of the hyperactive-impulsive subtype of ADHD. Lesions to the anterior cingulate or medial prefrontal cortex, two afferents to the AcbC, do not induce impulsive choice, but lesions of the basolateral amygdala do, while lesions to the orbitofrontal cortex have had opposite effects in different tasks measuring impulsive choice. In theory, impulsive choice may emerge as a result of abnormal processing of the magnitude of rewards, or as a result of a deficit in the effects of delayed reinforcement. Recent evidence suggests that AcbC-lesioned rats perceive reward magnitude normally, but exhibit a selective deficit in learning instrumental responses using delayed reinforcement, suggesting that the AcbC is a reinforcement learning system that mediates the effects of delayed rewards.</description>
    <dc:title>Limbic corticostriatal systems and delayed reinforcement.</dc:title>

    <dc:creator>RN Cardinal</dc:creator>
    <dc:creator>CA Winstanley</dc:creator>
    <dc:creator>TW Robbins</dc:creator>
    <dc:creator>BJ Everitt</dc:creator>
    <dc:identifier>doi:10.1196/annals.1308.004</dc:identifier>
    <dc:source>Ann N Y Acad Sci, Vol. 1021 (June 2004), pp. 33-50.</dc:source>
    <dc:date>2005-03-04T18:19:21-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>Ann N Y Acad Sci</prism:publicationName>
    <prism:issn>0077-8923</prism:issn>
    <prism:volume>1021</prism:volume>
    <prism:startingPage>33</prism:startingPage>
    <prism:endingPage>50</prism:endingPage>
    <prism:category>discounting</prism:category>
    <prism:category>_note</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/klouie/article/460432">
    <title>Nucleus accumbens neurons are innately tuned for rewarding and aversive taste stimuli, encode their predictors, and are linked to motor output.</title>
    <link>http://www.citeulike.org/user/klouie/article/460432</link>
    <description>&lt;i&gt;Neuron, Vol. 45, No. 4. (17 February 2005), pp. 587-597.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The nucleus accumbens (NAc) is a key component of the brain's reward pathway, yet little is known of how NAc cells respond to primary rewarding or aversive stimuli. Here, naive rats received brief intraoral infusions of sucrose and quinine paired with cues in a classical conditioning paradigm while the electrophysiological activity of individual NAc neurons was recorded. NAc neurons (102) were typically inhibited by sucrose (39 of 52, 75%) or excited by quinine (30 of 40, 75%) infusions. Changes in firing rate were correlated with the oromotor response to intraoral infusions. Most taste-responsive neurons responded to only one of the stimuli. NAc neurons developed responses to the cues paired with sucrose and quinine. Thus, NAc neurons are innately tuned to rewarding and aversive stimuli and rapidly develop responses to predictive cues. The results indicate that the output of the NAc is very different when rats taste rewarding versus aversive stimuli.</description>
    <dc:title>Nucleus accumbens neurons are innately tuned for rewarding and aversive taste stimuli, encode their predictors, and are linked to motor output.</dc:title>

    <dc:creator>MF Roitman</dc:creator>
    <dc:creator>RA Wheeler</dc:creator>
    <dc:creator>RM Carelli</dc:creator>
    <dc:identifier>doi:10.1016/j.neuron.2004.12.055</dc:identifier>
    <dc:source>Neuron, Vol. 45, No. 4. (17 February 2005), pp. 587-597.</dc:source>
    <dc:date>2006-01-09T22:58:17-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Neuron</prism:publicationName>
    <prism:issn>0896-6273</prism:issn>
    <prism:volume>45</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>587</prism:startingPage>
    <prism:endingPage>597</prism:endingPage>
    <prism:category>aversive</prism:category>
    <prism:category>electrophysiology</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>rat</prism:category>
    <prism:category>reward</prism:category>
    <prism:category>ventral_striatum</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/klouie/article/176926">
    <title>Subsecond dopamine release promotes cocaine seeking.</title>
    <link>http://www.citeulike.org/user/klouie/article/176926</link>
    <description>&lt;i&gt;Nature, Vol. 422, No. 6932. (10 April 2003), pp. 614-618.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The dopamine-containing projection from the ventral tegmental area of the midbrain to the nucleus accumbens is critically involved in mediating the reinforcing properties of cocaine. Although neurons in this area respond to rewards on a subsecond timescale, neurochemical studies have only addressed the role of dopamine in drug addiction by examining changes in the tonic (minute-to-minute) levels of extracellular dopamine. To investigate the role of phasic (subsecond) dopamine signalling, we measured dopamine every 100 ms in the nucleus accumbens using electrochemical technology. Rapid changes in extracellular dopamine concentration were observed at key aspects of drug-taking behaviour in rats. Before lever presses for cocaine, there was an increase in dopamine that coincided with the initiation of drug-seeking behaviours. Notably, these behaviours could be reproduced by electrically evoking dopamine release on this timescale. After lever presses, there were further increases in dopamine concentration at the concurrent presentation of cocaine-related cues. These cues alone also elicited similar, rapid dopamine signalling, but only in animals where they had previously been paired to cocaine delivery. These findings reveal an unprecedented role for dopamine in the regulation of drug taking in real time.</description>
    <dc:title>Subsecond dopamine release promotes cocaine seeking.</dc:title>

    <dc:creator>PE Phillips</dc:creator>
    <dc:creator>GD Stuber</dc:creator>
    <dc:creator>ML Heien</dc:creator>
    <dc:creator>RM Wightman</dc:creator>
    <dc:creator>RM Carelli</dc:creator>
    <dc:identifier>doi:10.1038/nature01476</dc:identifier>
    <dc:source>Nature, Vol. 422, No. 6932. (10 April 2003), pp. 614-618.</dc:source>
    <dc:date>2005-05-03T05:03:17-00:00</dc:date>
    <prism:publicationYear>2003</prism:publicationYear>
    <prism:publicationName>Nature</prism:publicationName>
    <prism:issn>0028-0836</prism:issn>
    <prism:volume>422</prism:volume>
    <prism:number>6932</prism:number>
    <prism:startingPage>614</prism:startingPage>
    <prism:endingPage>618</prism:endingPage>
    <prism:category>cyclic_voltammetry</prism:category>
    <prism:category>dopamine</prism:category>
    <prism:category>microstimulation</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>rat</prism:category>
    <prism:category>reward</prism:category>
    <prism:category>vta</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/klouie/article/141994">
    <title>Nucleus accumbens core lesions retard instrumental learning and performance with delayed reinforcement in the rat.</title>
    <link>http://www.citeulike.org/user/klouie/article/141994</link>
    <description>&lt;i&gt;BMC Neurosci, Vol. 6, No. 1. (3 February 2005)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: Delays between actions and their outcomes severely hinder reinforcement learning systems, but little is known of the neural mechanism by which animals overcome this problem and bridge such delays. The nucleus accumbens core (AcbC), part of the ventral striatum, is required for normal preference for a large, delayed reward over a small, immediate reward (self-controlled choice) in rats, but the reason for this is unclear. We investigated the role of the AcbC in learning a free-operant instrumental response using delayed reinforcement, performance of a previously-learned response for delayed reinforcement, and assessment of the relative magnitudes of two different rewards. RESULTS: Groups of rats with excitotoxic or sham lesions of the AcbC acquired an instrumental response with different delays (0, 10, or 20 s) between the lever-press response and reinforcer delivery. A second (inactive) lever was also present, but responding on it was never reinforced. As expected, the delays retarded learning in normal rats. AcbC lesions did not hinder learning in the absence of delays, but AcbC-lesioned rats were impaired in learning when there was a delay, relative to sham-operated controls. All groups eventually acquired the response and discriminated the active lever from the inactive lever to some degree. Rats were subsequently trained to discriminate reinforcers of different magnitudes. AcbC-lesioned rats were more sensitive to differences in reinforcer magnitude than sham-operated controls, suggesting that the deficit in self-controlled choice previously observed in such rats was a consequence of reduced preference for delayed rewards relative to immediate rewards, not of reduced preference for large rewards relative to small rewards. AcbC lesions also impaired the performance of a previously-learned instrumental response in a delay-dependent fashion. CONCLUSIONS: These results demonstrate that the AcbC contributes to instrumental learning and performance by bridging delays between subjects' actions and the ensuing outcomes that reinforce behaviour.</description>
    <dc:title>Nucleus accumbens core lesions retard instrumental learning and performance with delayed reinforcement in the rat.</dc:title>

    <dc:creator>RN Cardinal</dc:creator>
    <dc:creator>TH Cheung</dc:creator>
    <dc:identifier>doi:10.1186/1471-2202-6-9</dc:identifier>
    <dc:source>BMC Neurosci, Vol. 6, No. 1. (3 February 2005)</dc:source>
    <dc:date>2005-03-28T16:05:40-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>BMC Neurosci</prism:publicationName>
    <prism:issn>1471-2202</prism:issn>
    <prism:volume>6</prism:volume>
    <prism:number>1</prism:number>
    <prism:category>choicebehavior</prism:category>
    <prism:category>discounting</prism:category>
    <prism:category>lesion</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>rat</prism:category>
    <prism:category>reward</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/klouie/article/851213">
    <title>The Nucleus Accumbens and Reward: Neurophysiological Investigations in Behaving Animals</title>
    <link>http://www.citeulike.org/user/klouie/article/851213</link>
    <description>&lt;i&gt;Behav Cogn Neurosci Rev, Vol. 1, No. 4. (1 December 2002), pp. 281-296.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The nucleus accumbens (Acb) is a crucial component of the brain reward system. This report reviews electrophysiological studies that examined Acb cell firing during goal-directed behaviors for natural reinforcers (food, water, sucrose) and drugs of abuse (cocaine, heroin, ethanol). Studies that examined the role of environmental stimuli and operant contingencies on Acb activity during behavior are also explored. Given the extensive literature that links dopamine in the Acb with drug reinforcement, experiments are considered that examined the influence of dopamine in modulating Acb cell firing during drug-seeking behaviors. Finally, because the Acb is one neural substrate of a larger brain reward circuit, the influence of afferent input (hippocampus and prefrontal cortex) on Acb cell firing during behavior is also discussed. These findings provide a unique insight into the cellular mechanisms underlying reward-related processing and goal-directed behaviors and reveal a level of functional organization in the Acb not identified by other experimental approaches. 10.1177/1534582302238338</description>
    <dc:title>The Nucleus Accumbens and Reward: Neurophysiological Investigations in Behaving Animals</dc:title>

    <dc:creator>Regina Carelli</dc:creator>
    <dc:identifier>doi:10.1177/1534582302238338</dc:identifier>
    <dc:source>Behav Cogn Neurosci Rev, Vol. 1, No. 4. (1 December 2002), pp. 281-296.</dc:source>
    <dc:date>2006-09-20T13:23:10-00:00</dc:date>
    <prism:publicationYear>2002</prism:publicationYear>
    <prism:publicationName>Behav Cogn Neurosci Rev</prism:publicationName>
    <prism:volume>1</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>281</prism:startingPage>
    <prism:endingPage>296</prism:endingPage>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>review</prism:category>
    <prism:category>reward</prism:category>
    <prism:category>ventral_striatum</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/klouie/article/598867">
    <title>Forebrain substrates of reward and motivation.</title>
    <link>http://www.citeulike.org/user/klouie/article/598867</link>
    <description>&lt;i&gt;J Comp Neurol, Vol. 493, No. 1. (5 December 2005), pp. 115-121.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Electrical stimulation of the medial forebrain bundle can reward arbitrary acts or motivate biologically primitive, species-typical behaviors like feeding or copulation. The subsystems involved in these behaviors are only partially characterized, but they appear to transsynaptically activate the mesocorticolimbic dopamine system. Basal function of the dopamine system is essential for arousal and motor function; phasic activation of this system is rewarding and can potentiate the effectiveness of reward-predictors that guide learned behaviors. This system is phasically activated by most drugs of abuse and such activation contributes to the habit-forming actions of these drugs.</description>
    <dc:title>Forebrain substrates of reward and motivation.</dc:title>

    <dc:creator>RA Wise</dc:creator>
    <dc:identifier>doi:10.1002/cne.20689</dc:identifier>
    <dc:source>J Comp Neurol, Vol. 493, No. 1. (5 December 2005), pp. 115-121.</dc:source>
    <dc:date>2006-04-24T21:07:39-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>J Comp Neurol</prism:publicationName>
    <prism:issn>0021-9967</prism:issn>
    <prism:volume>493</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>115</prism:startingPage>
    <prism:endingPage>121</prism:endingPage>
    <prism:category>dopamine</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>review</prism:category>
    <prism:category>reward</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/klouie/article/868270">
    <title>The nucleus accumbens as part of a basal ganglia action selection circuit.</title>
    <link>http://www.citeulike.org/user/klouie/article/868270</link>
    <description>&lt;i&gt;Psychopharmacology (Berl) (16 September 2006)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: The nucleus accumbens is the ventral extent of the striatum, the main input nucleus of the basal ganglia. Recent hypotheses propose that the accumbens and its dopamine projection from the midbrain contribute to appetitive behaviors required to obtain reward. However, the specific nature of this contribution is unclear. In contrast, significant advances have been made in understanding the role of the dorsal striatum in action selection and decision making. OBJECTIVE: In order to develop a hypothesis of the role of nucleus accumbens dopamine in action selection, the physiology and behavioral pharmacology of the nucleus accumbens are compared to those of the dorsal striatum. HYPOTHESES: Three hypotheses concerning the role of dopamine in these structures are proposed: (1) that dopamine release in the dorsal striatum serves to facilitate the ability to respond appropriately to temporally predictable stimuli (that is, stimuli that are so predictable that animals engage in anticipatory behavior just prior to the stimulus); (2) that dopamine in the nucleus accumbens facilitates the ability to respond to temporally unpredictable stimuli (which require interruption of ongoing behavior); and (3) that accumbens neurons participate in action selection in response to such stimuli by virtue of their direct (monosynaptic inhibitory) and indirect (polysynaptic excitatory) projections to basal ganglia output nuclei.</description>
    <dc:title>The nucleus accumbens as part of a basal ganglia action selection circuit.</dc:title>

    <dc:creator>Saleem Nicola</dc:creator>
    <dc:identifier>doi:10.1007/s00213-006-0510-4</dc:identifier>
    <dc:source>Psychopharmacology (Berl) (16 September 2006)</dc:source>
    <dc:date>2006-09-25T18:19:07-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Psychopharmacology (Berl)</prism:publicationName>
    <prism:issn>0033-3158</prism:issn>
    <prism:category>basal_ganglia</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>review</prism:category>
    <prism:category>ventral_striatum</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/klouie/article/113748">
    <title>Impulsive Choice Induced in Rats by Lesions of the Nucleus Accumbens Core</title>
    <link>http://www.citeulike.org/user/klouie/article/113748</link>
    <description>&lt;i&gt;Science, Vol. 292, No. 5526. (29 June 2001), pp. 2499-2501.&lt;/i&gt;</description>
    <dc:title>Impulsive Choice Induced in Rats by Lesions of the Nucleus Accumbens Core</dc:title>

    <dc:creator>Rudolf Cardinal</dc:creator>
    <dc:creator>David Pennicott</dc:creator>
    <dc:creator>Lakmali Sugathapala</dc:creator>
    <dc:creator>Trevor Robbins</dc:creator>
    <dc:creator>Barry Everitt</dc:creator>
    <dc:identifier>doi:10.1126/science.1060818</dc:identifier>
    <dc:source>Science, Vol. 292, No. 5526. (29 June 2001), pp. 2499-2501.</dc:source>
    <dc:date>2005-03-03T22:25:12-00:00</dc:date>
    <prism:publicationYear>2001</prism:publicationYear>
    <prism:publicationName>Science</prism:publicationName>
    <prism:volume>292</prism:volume>
    <prism:number>5526</prism:number>
    <prism:startingPage>2499</prism:startingPage>
    <prism:endingPage>2501</prism:endingPage>
    <prism:category>choicebehavior</prism:category>
    <prism:category>discounting</prism:category>
    <prism:category>lesion</prism:category>
    <prism:category>_note</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>rat</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/klouie/article/455012">
    <title>Convergence and segregation of ventral striatal inputs and outputs.</title>
    <link>http://www.citeulike.org/user/klouie/article/455012</link>
    <description>&lt;i&gt;Ann N Y Acad Sci, Vol. 877 (29 June 1999), pp. 49-63.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The ventral striatum, which prominently includes the nucleus accumbens (Acb), is a heterogeneous area. Within the Acb of rats, a peripherally located shell and a centrally situated core can be recognized that have different connectional, neurochemical, and functional identities. Although the Acb core resembles in many respects the dorsally adjacent caudate-putamen complex in its striatal character, the Acb shell has, in addition to striatal features, a more diverse array of neurochemical characteristics, and afferent and efferent connections. Inputs and outputs of the Acb, in particular of the shell, are inhomogeneously distributed, resulting in a mosaical arrangement of concentrations of afferent fibers and terminals and clusters of output neurons. To determine the precise relationships between the distributional patterns of various afferents (e.g., from the prefrontal cortex, the basal amygdaloid complex, the hippocampal formation, and the midline/intralaminar thalamic nuclei) and efferents to the ventral pallidum and mesencephalon, neuroanatomical anterograde and retrograde tracing experiments were carried out. The results of the double anterograde, double retrograde, and anterograde/retrograde tracing experiments indicate that various parts of the shell (dorsomedial, ventromedial, ventral, and lateral) and the core (medial and lateral) have different input-output characteristics. Furthermore, within these Acb regions, various populations of neurons can be identified, arranged in a cluster-like fashion, onto which specific sets of afferents converge and that project to particular output stations, distinct from the input-output relationships of neighboring, cluster-like neuronal populations. These results support the idea that the nucleus accumbens may consist of a collection of neuronal ensembles with different input-output relationships and, presumably, different functional characteristics.</description>
    <dc:title>Convergence and segregation of ventral striatal inputs and outputs.</dc:title>

    <dc:creator>HJ Groenewegen</dc:creator>
    <dc:creator>CI Wright</dc:creator>
    <dc:creator>AV Beijer</dc:creator>
    <dc:creator>P Voorn</dc:creator>
    <dc:source>Ann N Y Acad Sci, Vol. 877 (29 June 1999), pp. 49-63.</dc:source>
    <dc:date>2006-01-03T19:04:09-00:00</dc:date>
    <prism:publicationYear>1999</prism:publicationYear>
    <prism:publicationName>Ann N Y Acad Sci</prism:publicationName>
    <prism:issn>0077-8923</prism:issn>
    <prism:volume>877</prism:volume>
    <prism:startingPage>49</prism:startingPage>
    <prism:endingPage>63</prism:endingPage>
    <prism:category>neuroanatomy</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>ventral_striatum</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/klouie/article/461193">
    <title>Cue-evoked firing of nucleus accumbens neurons encodes motivational significance during a discriminative stimulus task.</title>
    <link>http://www.citeulike.org/user/klouie/article/461193</link>
    <description>&lt;i&gt;J Neurophysiol, Vol. 91, No. 4. (April 2004), pp. 1840-1865.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The nucleus accumbens (NAc) has long been thought of as a limbic-motor interface. Despite behavioral and anatomical evidence in favor of this idea, little is known about how NAc neurons encode information about motivationally relevant environmental cues and use this information to affect motor action. We therefore investigated the firing of these neurons during the performance of a discriminative stimulus (DS) task using simultaneous multiple single-unit recordings in rats. In this task, two stimuli are randomly presented to the animal: a DS, which signals the availability of a sucrose reward contingent on an operant response, and a similar but nonrewarded stimulus (NS). Subpopulations of NAc neurons increased or decreased their firing in association with several distinct components of the task. In this paper, we investigate cue- and operant-responsive neurons. Neurons excited and inhibited by cues showed larger firing changes in response to the DS than the NS and larger changes when the animal made an operant response to the cue than when the animal failed to respond. Excitations during operant responding were not modulated by the information contained by the cue, whereas inhibitions during operant responding were somewhat larger if the operant response occurred during the DS and somewhat smaller if they occurred in the absence of a cue. These results are consistent with the hypothesis that the firing of subpopulations of NAc neurons encode both the predictive value of environmental stimuli and the specific motor behaviors required to respond to them.</description>
    <dc:title>Cue-evoked firing of nucleus accumbens neurons encodes motivational significance during a discriminative stimulus task.</dc:title>

    <dc:creator>SM Nicola</dc:creator>
    <dc:creator>IA Yun</dc:creator>
    <dc:creator>KT Wakabayashi</dc:creator>
    <dc:creator>HL Fields</dc:creator>
    <dc:identifier>doi:10.1152/jn.00657.2003</dc:identifier>
    <dc:source>J Neurophysiol, Vol. 91, No. 4. (April 2004), pp. 1840-1865.</dc:source>
    <dc:date>2006-01-10T17:37:07-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>J Neurophysiol</prism:publicationName>
    <prism:issn>0022-3077</prism:issn>
    <prism:volume>91</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>1840</prism:startingPage>
    <prism:endingPage>1865</prism:endingPage>
    <prism:category>electrophysiology</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>rat</prism:category>
    <prism:category>reward</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/klouie/article/455011">
    <title>Neural signals in the monkey ventral striatum related to motivation for juice and cocaine rewards.</title>
    <link>http://www.citeulike.org/user/klouie/article/455011</link>
    <description>&lt;i&gt;J Neurophysiol, Vol. 75, No. 3. (March 1996), pp. 1061-1073.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;1. The results of neuropsychological, neuropharmacological, and neurophysiological experiments have implicated the ventral striatum in reward-related processes. We designed a task to allow us to separate the effects of sensory, motor, and internal signals so that we could study the correlation between the activity of neurons in the ventral striatum and different motivational states. In this task, a visual stimulus was used to cue the monkeys as to their progress toward earning a reward. The monkeys performed more quickly and with fewer mistakes in the rewarded trials. After analyzing the behavioral results from three monkeys, we recorded from 143 neurons from two of the monkeys while they performed the task with either juice or cocaine reward. 2. In this task the monkey was required to release its grip on a bar when a small visual response cue changed colors from red (the wait signal) to green (the go signal). The duration of the wait signal was varied randomly. The cue became blue whenever the monkey successfully responded to the go signal within 1 s of its appearance. A reward was delivered after the monkey successfully completed one, two, or three trials. The schedules were randomly interleaved. A second visual stimulus that progressively brightened or dimmed signaled to the monkeys their progress toward earning a reward. This discriminative cue allowed the monkeys to judge the proportion of work remaining in the current ratio schedule of reinforcement. Data were collected from three monkeys while they performed this task. 3. The average reaction times became faster and error rates declined as the monkeys progressed toward completing the current schedule of reinforcement and thereby earning a reward, whereas the modal reaction time did not change. As the duration of the wait period before the go signal increased, the monkeys reacted more quickly but their error rates scarcely changed. From these results we infer that the effects of motivation and motor readiness in this task are generated by separate mechanisms rather than by a single mechanism subserving generalized arousal. 4. The activity of 138 ventral striatal neurons was sampled in two monkeys while they performed the task to earn juice reward. We saw tonic changes in activity throughout the trials, and we saw phasic activity following the reward. The activity of these neurons was markedly different during juice-rewarded trials than during correctly performed trials when no reward was forthcoming (or expected). The responses also were weakly, but significantly, related to the proximity of the reward in the schedules requiring more than one trial. 5. The monkeys worked to obtain intravenous cocaine while we recorded 62 neurons. For 57 of the neurons, we recorded activity while the monkeys worked in blocks of trials during which they self-administered cocaine after blocks during which they worked for juice. Although fewer neurons responded to cocaine than to juice reward (19 vs. 33%), this difference was not significant. The neuronal response properties to cocaine and juice rewards were independent; that is, the responses when one was the reward one failed to predict the response when the other was the reward. In addition, the neuronal activity lost most of its selectivity for rewarded trials, i.e, the activity did not distinguish nearly as well between cocaine and sham rewards as between juice and sham rewards. 6. Our results show that mechanisms by which cocaine acts do not appear to be the same as the ones activated when the monkeys were presented with an oral juice reward. This finding raises the intriguing possibility that the effects of cocaine could be reduced selectively without blocking the effects of many natural rewards.</description>
    <dc:title>Neural signals in the monkey ventral striatum related to motivation for juice and cocaine rewards.</dc:title>

    <dc:creator>EM Bowman</dc:creator>
    <dc:creator>TG Aigner</dc:creator>
    <dc:creator>BJ Richmond</dc:creator>
    <dc:source>J Neurophysiol, Vol. 75, No. 3. (March 1996), pp. 1061-1073.</dc:source>
    <dc:date>2006-01-03T19:02:13-00:00</dc:date>
    <prism:publicationYear>1996</prism:publicationYear>
    <prism:publicationName>J Neurophysiol</prism:publicationName>
    <prism:issn>0022-3077</prism:issn>
    <prism:volume>75</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>1061</prism:startingPage>
    <prism:endingPage>1073</prism:endingPage>
    <prism:category>cocaine</prism:category>
    <prism:category>electrophysiology</prism:category>
    <prism:category>monkey</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>_pg</prism:category>
    <prism:category>reward</prism:category>
    <prism:category>ventral_striatum</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/klouie/article/843643">
    <title>The nucleus accumbens as a complex of functionally distinct neuronal ensembles: an integration of behavioural, electrophysiological and anatomical data.</title>
    <link>http://www.citeulike.org/user/klouie/article/843643</link>
    <description>&lt;i&gt;Prog Neurobiol, Vol. 42, No. 6. (April 1994), pp. 719-761.&lt;/i&gt;</description>
    <dc:title>The nucleus accumbens as a complex of functionally distinct neuronal ensembles: an integration of behavioural, electrophysiological and anatomical data.</dc:title>

    <dc:creator>CM Pennartz</dc:creator>
    <dc:creator>HJ Groenewegen</dc:creator>
    <dc:creator>FH Lopes da Silva</dc:creator>
    <dc:source>Prog Neurobiol, Vol. 42, No. 6. (April 1994), pp. 719-761.</dc:source>
    <dc:date>2006-09-14T21:05:03-00:00</dc:date>
    <prism:publicationYear>1994</prism:publicationYear>
    <prism:publicationName>Prog Neurobiol</prism:publicationName>
    <prism:issn>0301-0082</prism:issn>
    <prism:volume>42</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>719</prism:startingPage>
    <prism:endingPage>761</prism:endingPage>
    <prism:category>neuroanatomy</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>review</prism:category>
    <prism:category>ventral_striatum</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/klouie/article/118543">
    <title>Reward processing in primate orbitofrontal cortex and basal ganglia.</title>
    <link>http://www.citeulike.org/user/klouie/article/118543</link>
    <description>&lt;i&gt;Cereb Cortex, Vol. 10, No. 3. (March 2000), pp. 272-284.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;This article reviews and interprets neuronal activities related to the expectation and delivery of reward in the primate orbitofrontal cortex, in comparison with slowly discharging neurons in the striatum (caudate, putamen and ventral striatum, including nucleus accumbens) and midbrain dopamine neurons. Orbitofrontal neurons showed three principal forms of reward-related activity during the performance of delayed response tasks, namely responses to reward-predicting instructions, activations during the expectation period immediately preceding reward and responses following reward. These activations discriminated between different rewards, often on the basis of the animals' preferences. Neurons in the striatum were also activated in relation to the expectation and detection of reward but in addition showed activities related to the preparation, initiation and execution of movements which reflected the expected reward. Dopamine neurons responded to rewards and reward-predicting stimuli, and coded an error in the prediction of reward. Thus, the investigated cortical and basal ganglia structures showed multiple, heterogeneous, partly simultaneous activations which were related to specific aspects of rewards. These activations may represent the neuronal substrates of rewards during learning and established behavioral performance. The processing of reward expectations suggests an access to central representations of rewards which may be used for the neuronal control of goaldirected behavior.</description>
    <dc:title>Reward processing in primate orbitofrontal cortex and basal ganglia.</dc:title>

    <dc:creator>W Schultz</dc:creator>
    <dc:creator>L Tremblay</dc:creator>
    <dc:creator>JR Hollerman</dc:creator>
    <dc:source>Cereb Cortex, Vol. 10, No. 3. (March 2000), pp. 272-284.</dc:source>
    <dc:date>2005-03-09T17:01:10-00:00</dc:date>
    <prism:publicationYear>2000</prism:publicationYear>
    <prism:publicationName>Cereb Cortex</prism:publicationName>
    <prism:issn>1047-3211</prism:issn>
    <prism:volume>10</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>272</prism:startingPage>
    <prism:endingPage>284</prism:endingPage>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>orbitofrontal</prism:category>
    <prism:category>review</prism:category>
    <prism:category>reward</prism:category>
    <prism:category>striatum</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/klouie/article/87212">
    <title>Functional microcircuitry in the accumbens underlying drug addiction: insights from real-time signaling during behavior</title>
    <link>http://www.citeulike.org/user/klouie/article/87212</link>
    <description>&lt;i&gt;Current Opinion in Neurobiology, Vol. 14, No. 6. (December 2004), pp. 763-768.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;An understanding of the neurobiological basis of drug addiction requires examination of real-time (subsecond) cellular and chemical responses in the brain reward system during drug-seeking and drug-taking behavior. Electrophysiological and electrochemical studies in the rodent nucleus accumbens have examined changes in cell firing and rapid dopamine signaling during crucial periods of behavioral responding for drugs, and show the associative nature of those signals. These findings are considered with respect to the functional microcircuitry in the nucleus accumbens that underlies goal-directed behavior and the role of this circuit in drug addiction.</description>
    <dc:title>Functional microcircuitry in the accumbens underlying drug addiction: insights from real-time signaling during behavior</dc:title>

    <dc:creator>Regina Carelli</dc:creator>
    <dc:creator>Mark Wightman</dc:creator>
    <dc:identifier>doi:10.1016/j.conb.2004.10.001</dc:identifier>
    <dc:source>Current Opinion in Neurobiology, Vol. 14, No. 6. (December 2004), pp. 763-768.</dc:source>
    <dc:date>2005-02-05T04:04:19-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>Current Opinion in Neurobiology</prism:publicationName>
    <prism:volume>14</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>763</prism:startingPage>
    <prism:endingPage>768</prism:endingPage>
    <prism:category>cyclic_voltammetry</prism:category>
    <prism:category>nucleus_accumbens</prism:category>
    <prism:category>rat</prism:category>
    <prism:category>review</prism:category>
    <prism:category>reward</prism:category>
    <prism:category>ventral_striatum</prism:category>
</item>



</rdf:RDF>

