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D2R-mediated signaling orchestrates just motor components of learning is a conclusion that is potentially biased due to the practice of avoiding doses of drugs that induce catalepsy (and therefore measuring only partial blockade of dopamine D2Rs) and single administrations [e.g. [3]]. Quite possibly, the functional role of D2Rs in associative learning might be masked because of this concern about locomotor disruption [2,6,8]. Doses of raclopride as low as 0.5 mg/kg significantly disrupt motor behavior [25], although this peripheral dose is consistently used in learning paradigms [e.g. [6]]. One might then ask: \"How then could the role of D2Rs in associative learning be dissociated from motor behavior?\" Seminal experiments [26-28] have clearly demonstrated that repeated administration of catalepsy-inducing doses of D2R antagonists in rodents actually leads to a striking behavioral tolerance to catalepsy. These doses have been shown to occupy well over 80% of available D2Rs [29]. Future experiments measuring acquisition of associative learning in rodents that received chronic administration of D2R antagonists and demonstrated behavioral tolerance to their motor disrupting effects would be a logical test of this hypothesis. However, the realization that multiple dopamine receptor subtypes would be concurrently targeted with the presently commercially available antagonists, such as D2Rs, D3Rs, and D4Rs would have to be rectified. We would argue that the most parsimonious approach at this time is to utilize mice that have been genetically altered such that they are lacking one or both functional alleles of the specific receptor of interest. While they do have their limitations (e.g. developmental compensation and strain effects in mouse lines not backcrossed adequately to a parental strain for a minimum of 10 generations), use of our inbred (N20 generation) animals in the present study (where no differences in locomotor behavior were detected between D2R-/- and D2R+/+ mice; Figs. 1 \u00262) revealed a previously unappreciated role of D2R-mediated signaling in associative learning and attention that could not be measured with the currently available, acutely administered D2R antagonists."}

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Quite possibly, the functional role of D2Rs in associative learning might be masked because of this concern about locomotor disruption [2,6,8]. Doses of raclopride as low as 0.5 mg/kg significantly disrupt motor behavior [25], although this peripheral dose is consistently used in learning paradigms [e.g. [6]]. One might then ask: \"How then could the role of D2Rs in associative learning be dissociated from motor behavior?\" Seminal experiments [26-28] have clearly demonstrated that repeated administration of catalepsy-inducing doses of D2R antagonists in rodents actually leads to a striking behavioral tolerance to catalepsy. These doses have been shown to occupy well over 80% of available D2Rs [29]. Future experiments measuring acquisition of associative learning in rodents that received chronic administration of D2R antagonists and demonstrated behavioral tolerance to their motor disrupting effects would be a logical test of this hypothesis. However, the realization that multiple dopamine receptor subtypes would be concurrently targeted with the presently commercially available antagonists, such as D2Rs, D3Rs, and D4Rs would have to be rectified. We would argue that the most parsimonious approach at this time is to utilize mice that have been genetically altered such that they are lacking one or both functional alleles of the specific receptor of interest. While they do have their limitations (e.g. developmental compensation and strain effects in mouse lines not backcrossed adequately to a parental strain for a minimum of 10 generations), use of our inbred (N20 generation) animals in the present study (where no differences in locomotor behavior were detected between D2R-/- and D2R+/+ mice; Figs. 1 \u00262) revealed a previously unappreciated role of D2R-mediated signaling in associative learning and attention that could not be measured with the currently available, acutely administered D2R antagonists."}

{"project":"craft-ca-core-dev","denotations":[{"id":"T3609","span":{"begin":5,"end":8},"obj":"PR:000001177"},{"id":"T3610","span":{"begin":66,"end":74},"obj":"GO:0007612"},{"id":"T3611","span":{"begin":159,"end":164},"obj":"CHEBI:23888"},{"id":"T3612","span":{"begin":237,"end":245},"obj":"CHEBI:18243"},{"id":"T3613","span":{"begin":237,"end":250},"obj":"PR:000001177"},{"id":"T3614","span":{"begin":330,"end":334},"obj":"PR:000001177"},{"id":"T3615","span":{"begin":338,"end":358},"obj":"GO:0008306"},{"id":"T3616","span":{"begin":405,"end":414},"obj":"GO:0040011"},{"id":"T3617","span":{"begin":572,"end":580},"obj":"GO:0007612"},{"id":"T3618","span":{"begin":651,"end":655},"obj":"PR:000001177"},{"id":"T3619","span":{"begin":659,"end":679},"obj":"GO:0008306"},{"id":"T3620","span":{"begin":831,"end":834},"obj":"PR:000001177"},{"id":"T3621","span":{"begin":850,"end":857},"obj":"NCBITaxon:9989"},{"id":"T3622","span":{"begin":987,"end":991},"obj":"PR:000001177"},{"id":"T3623","span":{"begin":1042,"end":1062},"obj":"GO:0008306"},{"id":"T3624","span":{"begin":1066,"end":1073},"obj":"NCBITaxon:9989"},{"id":"T3625","span":{"begin":1114,"end":1117},"obj":"PR:000001177"},{"id":"T3626","span":{"begin":1285,"end":1293},"obj":"CHEBI:18243"},{"id":"T3627","span":{"begin":1406,"end":1410},"obj":"PR:000001177"},{"id":"T3628","span":{"begin":1412,"end":1416},"obj":"PR:000001178"},{"id":"T3629","span":{"begin":1422,"end":1426},"obj":"PR:000001179"},{"id":"T3630","span":{"begin":1533,"end":1537},"obj":"NCBITaxon:10088"},{"id":"T3631","span":{"begin":1553,"end":1564},"obj":"SO:0000704"},{"id":"T3632","span":{"begin":1623,"end":1630},"obj":"SO:0001023"},{"id":"T3633","span":{"begin":1761,"end":1766},"obj":"NCBITaxon:10088"},{"id":"T3634","span":{"begin":1890,"end":1897},"obj":"NCBITaxon:33208"},{"id":"T3635","span":{"begin":1944,"end":1962},"obj":"GO:0007626"},{"id":"T3636","span":{"begin":1985,"end":1988},"obj":"PR:000001177"},{"id":"T3637","span":{"begin":1996,"end":1999},"obj":"PR:000001177"},{"id":"T3638","span":{"begin":2003,"end":2007},"obj":"NCBITaxon:10088"},{"id":"T3639","span":{"begin":2065,"end":2068},"obj":"PR:000001177"},{"id":"T3640","span":{"begin":2091,"end":2111},"obj":"GO:0008306"},{"id":"T3641","span":{"begin":2204,"end":2207},"obj":"PR:000001177"}],"text":"That D2R-mediated signaling orchestrates just motor components of learning is a conclusion that is potentially biased due to the practice of avoiding doses of drugs that induce catalepsy (and therefore measuring only partial blockade of dopamine D2Rs) and single administrations [e.g. [3]]. Quite possibly, the functional role of D2Rs in associative learning might be masked because of this concern about locomotor disruption [2,6,8]. Doses of raclopride as low as 0.5 mg/kg significantly disrupt motor behavior [25], although this peripheral dose is consistently used in learning paradigms [e.g. [6]]. One might then ask: \"How then could the role of D2Rs in associative learning be dissociated from motor behavior?\" Seminal experiments [26-28] have clearly demonstrated that repeated administration of catalepsy-inducing doses of D2R antagonists in rodents actually leads to a striking behavioral tolerance to catalepsy. These doses have been shown to occupy well over 80% of available D2Rs [29]. Future experiments measuring acquisition of associative learning in rodents that received chronic administration of D2R antagonists and demonstrated behavioral tolerance to their motor disrupting effects would be a logical test of this hypothesis. However, the realization that multiple dopamine receptor subtypes would be concurrently targeted with the presently commercially available antagonists, such as D2Rs, D3Rs, and D4Rs would have to be rectified. We would argue that the most parsimonious approach at this time is to utilize mice that have been genetically altered such that they are lacking one or both functional alleles of the specific receptor of interest. While they do have their limitations (e.g. developmental compensation and strain effects in mouse lines not backcrossed adequately to a parental strain for a minimum of 10 generations), use of our inbred (N20 generation) animals in the present study (where no differences in locomotor behavior were detected between D2R-/- and D2R+/+ mice; Figs. 1 \u00262) revealed a previously unappreciated role of D2R-mediated signaling in associative learning and attention that could not be measured with the currently available, acutely administered D2R antagonists."}

{"project":"2_test","denotations":[{"id":"15061865-9329075-12857741","span":{"begin":286,"end":287},"obj":"9329075"},{"id":"15061865-12445713-12857742","span":{"begin":427,"end":428},"obj":"12445713"},{"id":"15061865-12629161-12857743","span":{"begin":429,"end":430},"obj":"12629161"},{"id":"15061865-12445722-12857744","span":{"begin":431,"end":432},"obj":"12445722"},{"id":"15061865-3615345-12857745","span":{"begin":513,"end":515},"obj":"3615345"},{"id":"15061865-12629161-12857746","span":{"begin":598,"end":599},"obj":"12629161"},{"id":"15061865-7197320-12857747","span":{"begin":738,"end":740},"obj":"7197320"},{"id":"15061865-556989-12857747","span":{"begin":738,"end":740},"obj":"556989"},{"id":"15061865-4277740-12857747","span":{"begin":738,"end":740},"obj":"4277740"},{"id":"15061865-11229973-12857748","span":{"begin":993,"end":995},"obj":"11229973"}],"text":"That D2R-mediated signaling orchestrates just motor components of learning is a conclusion that is potentially biased due to the practice of avoiding doses of drugs that induce catalepsy (and therefore measuring only partial blockade of dopamine D2Rs) and single administrations [e.g. [3]]. Quite possibly, the functional role of D2Rs in associative learning might be masked because of this concern about locomotor disruption [2,6,8]. Doses of raclopride as low as 0.5 mg/kg significantly disrupt motor behavior [25], although this peripheral dose is consistently used in learning paradigms [e.g. [6]]. One might then ask: \"How then could the role of D2Rs in associative learning be dissociated from motor behavior?\" Seminal experiments [26-28] have clearly demonstrated that repeated administration of catalepsy-inducing doses of D2R antagonists in rodents actually leads to a striking behavioral tolerance to catalepsy. These doses have been shown to occupy well over 80% of available D2Rs [29]. Future experiments measuring acquisition of associative learning in rodents that received chronic administration of D2R antagonists and demonstrated behavioral tolerance to their motor disrupting effects would be a logical test of this hypothesis. However, the realization that multiple dopamine receptor subtypes would be concurrently targeted with the presently commercially available antagonists, such as D2Rs, D3Rs, and D4Rs would have to be rectified. We would argue that the most parsimonious approach at this time is to utilize mice that have been genetically altered such that they are lacking one or both functional alleles of the specific receptor of interest. While they do have their limitations (e.g. developmental compensation and strain effects in mouse lines not backcrossed adequately to a parental strain for a minimum of 10 generations), use of our inbred (N20 generation) animals in the present study (where no differences in locomotor behavior were detected between D2R-/- and D2R+/+ mice; Figs. 1 \u00262) revealed a previously unappreciated role of D2R-mediated signaling in associative learning and attention that could not be measured with the currently available, acutely administered D2R antagonists."}