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Role of D1-like receptors in amphetamine-induced behavioral sensitization: a study using D1A receptor knockout mice.
Psychopharmacology (Berl). 2002 Feb; 159(4):407-14.P

Abstract

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.

Authors+Show Affiliations

Department of Psychology, California State University, San Bernadino, 92407, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11823893

Citation

Karper, Patrick E., et al. "Role of D1-like Receptors in Amphetamine-induced Behavioral Sensitization: a Study Using D1A Receptor Knockout Mice." Psychopharmacology, vol. 159, no. 4, 2002, pp. 407-14.
Karper PE, De la Rosa H, Newman ER, et al. Role of D1-like receptors in amphetamine-induced behavioral sensitization: a study using D1A receptor knockout mice. Psychopharmacology (Berl). 2002;159(4):407-14.
Karper, P. E., De la Rosa, H., Newman, E. R., Krall, C. M., Nazarian, A., McDougall, S. A., & Crawford, C. A. (2002). Role of D1-like receptors in amphetamine-induced behavioral sensitization: a study using D1A receptor knockout mice. Psychopharmacology, 159(4), 407-14.
Karper PE, et al. Role of D1-like Receptors in Amphetamine-induced Behavioral Sensitization: a Study Using D1A Receptor Knockout Mice. Psychopharmacology (Berl). 2002;159(4):407-14. PubMed PMID: 11823893.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of D1-like receptors in amphetamine-induced behavioral sensitization: a study using D1A receptor knockout mice. AU - Karper,Patrick E, AU - De la Rosa,Herminia, AU - Newman,Eva R, AU - Krall,Catherine M, AU - Nazarian,Arbi, AU - McDougall,Sanders A, AU - Crawford,Cynthia A, Y1 - 2001/11/20/ PY - 2001/04/30/received PY - 2001/09/10/accepted PY - 2002/2/2/pubmed PY - 2002/4/18/medline PY - 2002/2/2/entrez SP - 407 EP - 14 JF - Psychopharmacology JO - Psychopharmacology (Berl) VL - 159 IS - 4 N2 - 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. SN - 0033-3158 UR - https://www.unboundmedicine.com/medline/citation/11823893/Role_of_D1_like_receptors_in_amphetamine_induced_behavioral_sensitization:_a_study_using_D1A_receptor_knockout_mice_ L2 - https://dx.doi.org/10.1007/s00213-001-0936-7 DB - PRIME DP - Unbound Medicine ER -