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http://purl.uniprot.org/citations/11823893http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11823893http://www.w3.org/2000/01/rdf-schema#comment"

Rationale

The role played by D(1)-like receptors in amphetamine-induced behavioral sensitization has been examined using both the D(1)-like receptor antagonist, SCH 23390, and the D(1A) receptor knockout mouse (i.e. D(1A)-deficient mice). Studies using these two approaches have provided conflicting evidence about the importance of D(1)-like receptors for amphetamine-induced behavioral sensitization.

Objective

The purpose of the present study was to determine: (a) whether D(1A)-deficient mice exhibit amphetamine-induced locomotor sensitization after 3 and 17 drug abstinence days, and (b) whether SCH 23390, which binds to both D(1A) and D(1B) receptor subtypes, blocks development of amphetamine sensitization in wild-type and D(1A)-deficient mice.

Methods

In the first experiment, adult wild-type and D(1A)-deficient mice were injected with amphetamine (0, 1, 2, 4, or 8 mg/kg, IP) for 7 consecutive days. In the second experiment, wild-type and D(1A)-deficient mice were pretreated with SCH 23390 (0, 0.15, or 0.5 mg/kg, IP) 30 min prior to being injected with amphetamine (0 or 8 mg/kg, IP). After each daily amphetamine injection, mice were placed in activity chambers where distance traveled (i.e. horizontal locomotor activity) was measured for 60 min. On the test days, which occurred after 3 or 17 drug abstinence days, mice were injected with 1 mg/kg amphetamine and locomotion was measured for 120 min.

Results

Both wild-type and D(1A)-deficient mice exhibited amphetamine-induced locomotor sensitization. Pretreatment with 0.5 mg/kg SCH 23390 blocked the development of locomotor sensitization in wild-type mice, but did not alter the sensitized responding of D(1A)-deficient mice.

Conclusions

It appears that D(1)-like receptors are necessary for the development of amphetamine sensitization in wild-type mice, while neither the D(1A) nor D(1B) receptor subtypes are necessary for the amphetamine-induced locomotor sensitization of D(1A)-deficient mice. A possible explanation for these conflicting results is that D(1A)-deficient mice may have a compensatory mechanism (not involving D(1B) receptors) that allows them to exhibit amphetamine-induced behavioral sensitization in the absence of the D(1A) receptor."xsd:string
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http://purl.uniprot.org/citations/11823893http://purl.uniprot.org/core/author"Nazarian A."xsd:string
http://purl.uniprot.org/citations/11823893http://purl.uniprot.org/core/author"McDougall S.A."xsd:string
http://purl.uniprot.org/citations/11823893http://purl.uniprot.org/core/author"Crawford C.A."xsd:string
http://purl.uniprot.org/citations/11823893http://purl.uniprot.org/core/author"Karper P.E."xsd:string
http://purl.uniprot.org/citations/11823893http://purl.uniprot.org/core/author"De la Rosa H."xsd:string
http://purl.uniprot.org/citations/11823893http://purl.uniprot.org/core/author"Krall C.M."xsd:string
http://purl.uniprot.org/citations/11823893http://purl.uniprot.org/core/author"Newman E.R."xsd:string
http://purl.uniprot.org/citations/11823893http://purl.uniprot.org/core/date"2002"xsd:gYear
http://purl.uniprot.org/citations/11823893http://purl.uniprot.org/core/name"Psychopharmacology (Berl)"xsd:string
http://purl.uniprot.org/citations/11823893http://purl.uniprot.org/core/pages"407-414"xsd:string
http://purl.uniprot.org/citations/11823893http://purl.uniprot.org/core/title"Role of D1-like receptors in amphetamine-induced behavioral sensitization: a study using D1A receptor knockout mice."xsd:string
http://purl.uniprot.org/citations/11823893http://purl.uniprot.org/core/volume"159"xsd:string
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http://purl.uniprot.org/citations/11823893http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/11823893
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