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data further support the hypothesis that signaling mediated by dopamine D2Rs tunes D1R-mediated mesocorticolimbic output. Calabresi et al. [34] demonstrated that tetanic stimulation of dorsal striatum slices prepared from D2R-/- mice is associated with enhanced EPSP and as a result increased striatal synaptic efficacy. In contrast, stimulation of dorsal striatum slices from wild-type mice resulted in IPSP activity, long-term depression, and decreased neuronal activity of striatal efferents [34]. Carlsson and colleagues [35] have speculated that dopamine D2R stimulation in the striatum serves to \"brake\" or diminish excitatory corticostriatal signaling and plasticity. Indeed, perseverative behavior is associated with over activity of the dorsal striatum in rodents [36] and over activity of the caudate in patients with ADHD [37] and a strong inverse correlation of D2R binding with compulsive behavior has been reported [22]. Importantly, our data indicate that the poor performances displayed by the D2R-/- mice are manifestations of reversal learning deficits and not gross motivational or sensory impairments. We therefore argue that D2Rs participate in signaling or alerting the organism of learning contingency changes during reversal learning and sculpt ongoing goal-directed behavior."}

{"project":"craft-ca-core-ex-dev","denotations":[{"id":"T3982","span":{"begin":62,"end":71},"obj":"GO_EXT:cell_communication_or_signaling_or_signal_transduction"},{"id":"T3983","span":{"begin":84,"end":92},"obj":"CHEBI:18243"},{"id":"T3984","span":{"begin":84,"end":97},"obj":"PR_EXT:000001177"},{"id":"T3985","span":{"begin":104,"end":107},"obj":"PR_EXT:000001175"},{"id":"T3986","span":{"begin":206,"end":221},"obj":"UBERON:0005382"},{"id":"T3987","span":{"begin":243,"end":246},"obj":"PR_EXT:000001177"},{"id":"T3988","span":{"begin":246,"end":247},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T3989","span":{"begin":248,"end":249},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T3990","span":{"begin":250,"end":254},"obj":"NCBITaxon:10088"},{"id":"T3991","span":{"begin":314,"end":322},"obj":"UBERON:0002435"},{"id":"T3992","span":{"begin":323,"end":331},"obj":"GO:0045202"},{"id":"T3993","span":{"begin":370,"end":385},"obj":"UBERON:0005382"},{"id":"T3994","span":{"begin":398,"end":407},"obj":"SO_EXT:wild_type_entity_or_quality"},{"id":"T3995","span":{"begin":408,"end":412},"obj":"NCBITaxon:10088"},{"id":"T3996","span":{"begin":476,"end":484},"obj":"CL:0000540"},{"id":"T3997","span":{"begin":497,"end":505},"obj":"UBERON:0002435"},{"id":"T3998","span":{"begin":506,"end":515},"obj":"UBERON:0006798"},{"id":"T3999","span":{"begin":572,"end":580},"obj":"CHEBI:18243"},{"id":"T4000","span":{"begin":572,"end":584},"obj":"PR_EXT:000001177"},{"id":"T4001","span":{"begin":604,"end":612},"obj":"UBERON:0002435"},{"id":"T4002","span":{"begin":670,"end":679},"obj":"GO_EXT:cell_communication_or_signaling_or_signal_transduction"},{"id":"T4003","span":{"begin":718,"end":726},"obj":"GO_PATO_EXT:biological_behavior"},{"id":"T4004","span":{"begin":767,"end":782},"obj":"UBERON:0005382"},{"id":"T4005","span":{"begin":786,"end":793},"obj":"NCBITaxon:9989"},{"id":"T4006","span":{"begin":824,"end":831},"obj":"UBERON:0001873"},{"id":"T4007","span":{"begin":895,"end":898},"obj":"PR_EXT:000001177"},{"id":"T4008","span":{"begin":899,"end":906},"obj":"CHEMINF_GO_EXT:chemical_binding_or_bond_formation"},{"id":"T4009","span":{"begin":923,"end":931},"obj":"GO_PATO_EXT:biological_behavior"},{"id":"T4010","span":{"begin":1031,"end":1034},"obj":"PR_EXT:000001177"},{"id":"T4011","span":{"begin":1034,"end":1035},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T4012","span":{"begin":1036,"end":1037},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T4013","span":{"begin":1038,"end":1042},"obj":"NCBITaxon:10088"},{"id":"T4014","span":{"begin":1074,"end":1082},"obj":"GO:0007612"},{"id":"T4015","span":{"begin":1122,"end":1129},"obj":"GO_EXT:detection_or_sensing_of_stimulus"},{"id":"T4016","span":{"begin":1167,"end":1171},"obj":"PR_EXT:000001177"},{"id":"T4017","span":{"begin":1187,"end":1196},"obj":"GO_EXT:cell_communication_or_signaling_or_signal_transduction"},{"id":"T4018","span":{"begin":1213,"end":1221},"obj":"NCBITaxon:1"},{"id":"T4019","span":{"begin":1225,"end":1233},"obj":"GO:0007612"},{"id":"T4020","span":{"begin":1270,"end":1278},"obj":"GO:0007612"},{"id":"T4021","span":{"begin":1303,"end":1311},"obj":"GO_EXT:biological_direction_or_guidance"},{"id":"T4022","span":{"begin":1312,"end":1320},"obj":"GO_PATO_EXT:biological_behavior"}],"text":"Electrophysiological data further support the hypothesis that signaling mediated by dopamine D2Rs tunes D1R-mediated mesocorticolimbic output. Calabresi et al. [34] demonstrated that tetanic stimulation of dorsal striatum slices prepared from D2R-/- mice is associated with enhanced EPSP and as a result increased striatal synaptic efficacy. In contrast, stimulation of dorsal striatum slices from wild-type mice resulted in IPSP activity, long-term depression, and decreased neuronal activity of striatal efferents [34]. Carlsson and colleagues [35] have speculated that dopamine D2R stimulation in the striatum serves to \"brake\" or diminish excitatory corticostriatal signaling and plasticity. Indeed, perseverative behavior is associated with over activity of the dorsal striatum in rodents [36] and over activity of the caudate in patients with ADHD [37] and a strong inverse correlation of D2R binding with compulsive behavior has been reported [22]. Importantly, our data indicate that the poor performances displayed by the D2R-/- mice are manifestations of reversal learning deficits and not gross motivational or sensory impairments. We therefore argue that D2Rs participate in signaling or alerting the organism of learning contingency changes during reversal learning and sculpt ongoing goal-directed behavior."}

{"project":"craft-ca-core-dev","denotations":[{"id":"T3709","span":{"begin":84,"end":92},"obj":"CHEBI:18243"},{"id":"T3710","span":{"begin":84,"end":97},"obj":"PR:000001177"},{"id":"T3711","span":{"begin":104,"end":107},"obj":"PR:000001175"},{"id":"T3712","span":{"begin":206,"end":221},"obj":"UBERON:0005382"},{"id":"T3713","span":{"begin":243,"end":246},"obj":"PR:000001177"},{"id":"T3714","span":{"begin":250,"end":254},"obj":"NCBITaxon:10088"},{"id":"T3715","span":{"begin":314,"end":322},"obj":"UBERON:0002435"},{"id":"T3728","span":{"begin":895,"end":898},"obj":"PR:000001177"},{"id":"T3729","span":{"begin":1031,"end":1034},"obj":"PR:000001177"},{"id":"T3730","span":{"begin":1038,"end":1042},"obj":"NCBITaxon:10088"},{"id":"T3731","span":{"begin":1074,"end":1082},"obj":"GO:0007612"},{"id":"T3732","span":{"begin":1167,"end":1171},"obj":"PR:000001177"},{"id":"T3733","span":{"begin":1213,"end":1221},"obj":"NCBITaxon:1"},{"id":"T3716","span":{"begin":323,"end":331},"obj":"GO:0045202"},{"id":"T3717","span":{"begin":370,"end":385},"obj":"UBERON:0005382"},{"id":"T3718","span":{"begin":408,"end":412},"obj":"NCBITaxon:10088"},{"id":"T3719","span":{"begin":476,"end":484},"obj":"CL:0000540"},{"id":"T3720","span":{"begin":497,"end":505},"obj":"UBERON:0002435"},{"id":"T3721","span":{"begin":506,"end":515},"obj":"UBERON:0006798"},{"id":"T3722","span":{"begin":572,"end":580},"obj":"CHEBI:18243"},{"id":"T3723","span":{"begin":572,"end":584},"obj":"PR:000001177"},{"id":"T3724","span":{"begin":604,"end":612},"obj":"UBERON:0002435"},{"id":"T3725","span":{"begin":767,"end":782},"obj":"UBERON:0005382"},{"id":"T3726","span":{"begin":786,"end":793},"obj":"NCBITaxon:9989"},{"id":"T3727","span":{"begin":824,"end":831},"obj":"UBERON:0001873"},{"id":"T3734","span":{"begin":1225,"end":1233},"obj":"GO:0007612"},{"id":"T3735","span":{"begin":1270,"end":1278},"obj":"GO:0007612"}],"text":"Electrophysiological data further support the hypothesis that signaling mediated by dopamine D2Rs tunes D1R-mediated mesocorticolimbic output. Calabresi et al. [34] demonstrated that tetanic stimulation of dorsal striatum slices prepared from D2R-/- mice is associated with enhanced EPSP and as a result increased striatal synaptic efficacy. In contrast, stimulation of dorsal striatum slices from wild-type mice resulted in IPSP activity, long-term depression, and decreased neuronal activity of striatal efferents [34]. Carlsson and colleagues [35] have speculated that dopamine D2R stimulation in the striatum serves to \"brake\" or diminish excitatory corticostriatal signaling and plasticity. Indeed, perseverative behavior is associated with over activity of the dorsal striatum in rodents [36] and over activity of the caudate in patients with ADHD [37] and a strong inverse correlation of D2R binding with compulsive behavior has been reported [22]. Importantly, our data indicate that the poor performances displayed by the D2R-/- mice are manifestations of reversal learning deficits and not gross motivational or sensory impairments. We therefore argue that D2Rs participate in signaling or alerting the organism of learning contingency changes during reversal learning and sculpt ongoing goal-directed behavior."}

{"project":"2_test","denotations":[{"id":"15061865-9169514-12857756","span":{"begin":161,"end":163},"obj":"9169514"},{"id":"15061865-9169514-12857757","span":{"begin":517,"end":519},"obj":"9169514"},{"id":"15061865-11264457-12857758","span":{"begin":547,"end":549},"obj":"11264457"},{"id":"15061865-11144344-12857759","span":{"begin":795,"end":797},"obj":"11144344"},{"id":"15061865-10742158-12857760","span":{"begin":855,"end":857},"obj":"10742158"},{"id":"15061865-10484959-12857761","span":{"begin":951,"end":953},"obj":"10484959"}],"text":"Electrophysiological data further support the hypothesis that signaling mediated by dopamine D2Rs tunes D1R-mediated mesocorticolimbic output. Calabresi et al. [34] demonstrated that tetanic stimulation of dorsal striatum slices prepared from D2R-/- mice is associated with enhanced EPSP and as a result increased striatal synaptic efficacy. In contrast, stimulation of dorsal striatum slices from wild-type mice resulted in IPSP activity, long-term depression, and decreased neuronal activity of striatal efferents [34]. Carlsson and colleagues [35] have speculated that dopamine D2R stimulation in the striatum serves to \"brake\" or diminish excitatory corticostriatal signaling and plasticity. Indeed, perseverative behavior is associated with over activity of the dorsal striatum in rodents [36] and over activity of the caudate in patients with ADHD [37] and a strong inverse correlation of D2R binding with compulsive behavior has been reported [22]. Importantly, our data indicate that the poor performances displayed by the D2R-/- mice are manifestations of reversal learning deficits and not gross motivational or sensory impairments. We therefore argue that D2Rs participate in signaling or alerting the organism of learning contingency changes during reversal learning and sculpt ongoing goal-directed behavior."}