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study demonstrates that signaling by dopamine D2Rs does not mediate the hedonic value of reinforcers, supporting and refining earlier findings [1,2]. However, mice completely deficient in D2Rs demonstrated disrupted acquisition of discriminative stimulus relationships and an impaired ability to recognize changes in behavioral determinants. Therefore, we suggest that during associative learning or when unexpected reinforcement outcomes are modified (reversal learning) dopamine-driven reinforcement impulses involve signaling mediated by dopamine D2Rs. In the course of associative learning, striatal synapses [38] receive experience-driven gain [7], thus permitting newly established reinforcement-mediated signals to traverse ascending efferents en route to the frontal cortex, completing a functional limbic/motor circuit [39-41]. Possibly, the lack of dopamine D2R-mediated signaling prevents refinement of the corticostriatal reinforcement circuits in the brains of the D2R-/- mice, thus impairing their ability to form S+/S- contingencies and disengage inappropriate dopamine D1R-mediated associative responding when unexpected consequences to goal-directed behaviors happened. Consequently, we are compelled to conclude that the perseverative performance deficits demonstrated by the D2R-/- mice in the tasks used in the present study reveal a previously unreported role for D2Rs in associative and reversal learning."}

{"project":"craft-ca-core-ex-dev","denotations":[{"id":"T5815","span":{"begin":29,"end":38},"obj":"GO_EXT:cell_communication_or_signaling_or_signal_transduction"},{"id":"T5816","span":{"begin":42,"end":50},"obj":"CHEBI:18243"},{"id":"T5817","span":{"begin":42,"end":55},"obj":"PR_EXT:000001177"},{"id":"T5818","span":{"begin":164,"end":168},"obj":"NCBITaxon:10088"},{"id":"T5819","span":{"begin":193,"end":197},"obj":"PR_EXT:000001177"},{"id":"T5820","span":{"begin":322,"end":332},"obj":"GO_PATO_EXT:biological_behavior"},{"id":"T5821","span":{"begin":381,"end":401},"obj":"GO:0008306"},{"id":"T5822","span":{"begin":467,"end":475},"obj":"GO:0007612"},{"id":"T5823","span":{"begin":477,"end":485},"obj":"CHEBI:18243"},{"id":"T5824","span":{"begin":524,"end":533},"obj":"GO_EXT:cell_communication_or_signaling_or_signal_transduction"},{"id":"T5825","span":{"begin":546,"end":554},"obj":"CHEBI:18243"},{"id":"T5826","span":{"begin":546,"end":559},"obj":"PR_EXT:000001177"},{"id":"T5827","span":{"begin":578,"end":598},"obj":"GO:0008306"},{"id":"T5828","span":{"begin":600,"end":608},"obj":"UBERON:0002435"},{"id":"T5829","span":{"begin":609,"end":617},"obj":"GO:0045202"},{"id":"T5830","span":{"begin":746,"end":755},"obj":"UBERON:0006798"},{"id":"T5831","span":{"begin":772,"end":786},"obj":"UBERON:0001870"},{"id":"T5832","span":{"begin":812,"end":818},"obj":"UBERON:0000349"},{"id":"T5833","span":{"begin":819,"end":824},"obj":"GO_EXT:biological_movement_or_translocation_process"},{"id":"T5834","span":{"begin":864,"end":872},"obj":"CHEBI:18243"},{"id":"T5835","span":{"begin":864,"end":876},"obj":"PR_EXT:000001177"},{"id":"T5836","span":{"begin":886,"end":895},"obj":"GO_EXT:cell_communication_or_signaling_or_signal_transduction"},{"id":"T5837","span":{"begin":969,"end":975},"obj":"UBERON:0000955"},{"id":"T5838","span":{"begin":983,"end":986},"obj":"PR_EXT:000001177"},{"id":"T5839","span":{"begin":986,"end":987},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T5840","span":{"begin":988,"end":989},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T5841","span":{"begin":990,"end":994},"obj":"NCBITaxon:10088"},{"id":"T5842","span":{"begin":1081,"end":1089},"obj":"CHEBI:18243"},{"id":"T5843","span":{"begin":1081,"end":1093},"obj":"PR_EXT:000001175"},{"id":"T5844","span":{"begin":1115,"end":1125},"obj":"GO_EXT:reaction_or_response"},{"id":"T5845","span":{"begin":1163,"end":1171},"obj":"GO_EXT:biological_direction_or_guidance"},{"id":"T5846","span":{"begin":1172,"end":1181},"obj":"GO_PATO_EXT:biological_behavior"},{"id":"T5847","span":{"begin":1299,"end":1302},"obj":"PR_EXT:000001177"},{"id":"T5848","span":{"begin":1302,"end":1303},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T5849","span":{"begin":1304,"end":1305},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T5850","span":{"begin":1306,"end":1310},"obj":"NCBITaxon:10088"},{"id":"T5851","span":{"begin":1390,"end":1394},"obj":"PR_EXT:000001177"},{"id":"T5852","span":{"begin":1398,"end":1409},"obj":"_FRAGMENT"},{"id":"T5853","span":{"begin":1423,"end":1431},"obj":"GO:0008306"}],"relations":[{"id":"R3774","pred":"_lexicallyChainedTo","subj":"T5853","obj":"T5852"}],"text":"This study demonstrates that signaling by dopamine D2Rs does not mediate the hedonic value of reinforcers, supporting and refining earlier findings [1,2]. However, mice completely deficient in D2Rs demonstrated disrupted acquisition of discriminative stimulus relationships and an impaired ability to recognize changes in behavioral determinants. Therefore, we suggest that during associative learning or when unexpected reinforcement outcomes are modified (reversal learning) dopamine-driven reinforcement impulses involve signaling mediated by dopamine D2Rs. In the course of associative learning, striatal synapses [38] receive experience-driven gain [7], thus permitting newly established reinforcement-mediated signals to traverse ascending efferents en route to the frontal cortex, completing a functional limbic/motor circuit [39-41]. Possibly, the lack of dopamine D2R-mediated signaling prevents refinement of the corticostriatal reinforcement circuits in the brains of the D2R-/- mice, thus impairing their ability to form S+/S- contingencies and disengage inappropriate dopamine D1R-mediated associative responding when unexpected consequences to goal-directed behaviors happened. Consequently, we are compelled to conclude that the perseverative performance deficits demonstrated by the D2R-/- mice in the tasks used in the present study reveal a previously unreported role for D2Rs in associative and reversal learning."}

{"project":"craft-ca-core-dev","denotations":[{"id":"T5788","span":{"begin":42,"end":50},"obj":"CHEBI:18243"},{"id":"T5789","span":{"begin":42,"end":55},"obj":"PR:000001177"},{"id":"T5790","span":{"begin":164,"end":168},"obj":"NCBITaxon:10088"},{"id":"T5791","span":{"begin":193,"end":197},"obj":"PR:000001177"},{"id":"T5792","span":{"begin":381,"end":401},"obj":"GO:0008306"},{"id":"T5793","span":{"begin":467,"end":475},"obj":"GO:0007612"},{"id":"T5794","span":{"begin":477,"end":485},"obj":"CHEBI:18243"},{"id":"T5795","span":{"begin":546,"end":554},"obj":"CHEBI:18243"},{"id":"T5796","span":{"begin":546,"end":559},"obj":"PR:000001177"},{"id":"T5797","span":{"begin":578,"end":598},"obj":"GO:0008306"},{"id":"T5798","span":{"begin":600,"end":608},"obj":"UBERON:0002435"},{"id":"T5799","span":{"begin":609,"end":617},"obj":"GO:0045202"},{"id":"T5800","span":{"begin":746,"end":755},"obj":"UBERON:0006798"},{"id":"T5801","span":{"begin":772,"end":786},"obj":"UBERON:0001870"},{"id":"T5802","span":{"begin":812,"end":818},"obj":"UBERON:0000349"},{"id":"T5803","span":{"begin":864,"end":872},"obj":"CHEBI:18243"},{"id":"T5804","span":{"begin":864,"end":876},"obj":"PR:000001177"},{"id":"T5805","span":{"begin":969,"end":975},"obj":"UBERON:0000955"},{"id":"T5806","span":{"begin":983,"end":986},"obj":"PR:000001177"},{"id":"T5807","span":{"begin":990,"end":994},"obj":"NCBITaxon:10088"},{"id":"T5808","span":{"begin":1081,"end":1089},"obj":"CHEBI:18243"},{"id":"T5809","span":{"begin":1081,"end":1093},"obj":"PR:000001175"},{"id":"T5810","span":{"begin":1299,"end":1302},"obj":"PR:000001177"},{"id":"T5811","span":{"begin":1306,"end":1310},"obj":"NCBITaxon:10088"},{"id":"T5812","span":{"begin":1390,"end":1394},"obj":"PR:000001177"},{"id":"T5813","span":{"begin":1398,"end":1409},"obj":"_FRAGMENT"},{"id":"T5814","span":{"begin":1423,"end":1431},"obj":"GO:0008306"}],"relations":[{"id":"R3773","pred":"_lexicallyChainedTo","subj":"T5814","obj":"T5813"}],"text":"This study demonstrates that signaling by dopamine D2Rs does not mediate the hedonic value of reinforcers, supporting and refining earlier findings [1,2]. However, mice completely deficient in D2Rs demonstrated disrupted acquisition of discriminative stimulus relationships and an impaired ability to recognize changes in behavioral determinants. Therefore, we suggest that during associative learning or when unexpected reinforcement outcomes are modified (reversal learning) dopamine-driven reinforcement impulses involve signaling mediated by dopamine D2Rs. In the course of associative learning, striatal synapses [38] receive experience-driven gain [7], thus permitting newly established reinforcement-mediated signals to traverse ascending efferents en route to the frontal cortex, completing a functional limbic/motor circuit [39-41]. Possibly, the lack of dopamine D2R-mediated signaling prevents refinement of the corticostriatal reinforcement circuits in the brains of the D2R-/- mice, thus impairing their ability to form S+/S- contingencies and disengage inappropriate dopamine D1R-mediated associative responding when unexpected consequences to goal-directed behaviors happened. Consequently, we are compelled to conclude that the perseverative performance deficits demonstrated by the D2R-/- mice in the tasks used in the present study reveal a previously unreported role for D2Rs in associative and reversal learning."}

{"project":"2_test","denotations":[{"id":"15061865-9858756-12857762","span":{"begin":149,"end":150},"obj":"9858756"},{"id":"15061865-12445713-12857763","span":{"begin":151,"end":152},"obj":"12445713"},{"id":"15061865-11793342-12857764","span":{"begin":619,"end":621},"obj":"11793342"},{"id":"15061865-11027236-12857765","span":{"begin":655,"end":656},"obj":"11027236"},{"id":"15061865-10933217-12857766","span":{"begin":834,"end":836},"obj":"10933217"},{"id":"15061865-10731217-12857766","span":{"begin":834,"end":836},"obj":"10731217"}],"text":"This study demonstrates that signaling by dopamine D2Rs does not mediate the hedonic value of reinforcers, supporting and refining earlier findings [1,2]. However, mice completely deficient in D2Rs demonstrated disrupted acquisition of discriminative stimulus relationships and an impaired ability to recognize changes in behavioral determinants. Therefore, we suggest that during associative learning or when unexpected reinforcement outcomes are modified (reversal learning) dopamine-driven reinforcement impulses involve signaling mediated by dopamine D2Rs. In the course of associative learning, striatal synapses [38] receive experience-driven gain [7], thus permitting newly established reinforcement-mediated signals to traverse ascending efferents en route to the frontal cortex, completing a functional limbic/motor circuit [39-41]. Possibly, the lack of dopamine D2R-mediated signaling prevents refinement of the corticostriatal reinforcement circuits in the brains of the D2R-/- mice, thus impairing their ability to form S+/S- contingencies and disengage inappropriate dopamine D1R-mediated associative responding when unexpected consequences to goal-directed behaviors happened. Consequently, we are compelled to conclude that the perseverative performance deficits demonstrated by the D2R-/- mice in the tasks used in the present study reveal a previously unreported role for D2Rs in associative and reversal learning."}