Role of D 1 -like receptors in amphetamine-induced behavioral sensitization: a study using D 1A receptor knockout mice

Karper, Patrick E.; Rosa, Herminia De La; Newman, Eva R.; Krall, Catherine M.; Nazarian, Arbi; McDougall, Sanders A.; Crawford, Cynthia A.

doi:10.1007/s00213-001-0936-7

Cited by 40 publications

(32 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Results in D1R knockout mice appear somewhat contradictory since locomotor sensitization induced by cocaine was strongly reduced, as expected, whereas locomotor sensitization to D-amph and cocaineinduced CPP were clearly obtained in these mice (Crawford et al, 1997;Karper et al, 2002;Xu et al, 2000). This apparent discrepancy may be related to the existence of compensatory mechanisms in D1R knockout mice (Karper et al, 2002;Stanwood et al, 2005). Our results show that the partial deficiency of D1R signaling does not prevent the development and the expression of locomotor sensitization to cocaine and D-amph.…”

Section: Gaolf and Not D1r Levels Control Acute Locomotor Effects Of mentioning

confidence: 41%

“…Similarly, both acquisition and expression of CPP with D-amph and cocaine were prevented by a D1R antagonist (Baker et al, 1998;Cervo and Samanin, 1995;Hiroi and White, 1991). Results in D1R knockout mice appear somewhat contradictory since locomotor sensitization induced by cocaine was strongly reduced, as expected, whereas locomotor sensitization to D-amph and cocaineinduced CPP were clearly obtained in these mice (Crawford et al, 1997;Karper et al, 2002;Xu et al, 2000). This apparent discrepancy may be related to the existence of compensatory mechanisms in D1R knockout mice (Karper et al, 2002;Stanwood et al, 2005).…”

Section: Gaolf and Not D1r Levels Control Acute Locomotor Effects Of mentioning

confidence: 79%

“…Dopamine acts on two types of G-proteincoupled receptors, the D1-type receptors (D1 and D5) and D2-type receptors (D2, D3, D4), which activate and inhibit adenylyl cyclase (AC), respectively. Although dopamine D1 receptors (D1R) signaling was consistently reported to be essential for acute responses to psychostimulants, its role in delayed responses is more controversial since divergent results were obtained in D1R antagonist-treated animals and in D1R knockout mice (Crawford et al, 1997;Karper et al, 2002;Xu et al, 2000). In the striatum D1R is coupled to AC through a specific G protein alpha subunit, Gaolf, whereas in other brain regions including the cerebral cortex, it is coupled through Gas, the quasiubiquitous isoform Zhuang et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Quantitative Changes in Gαolf Protein Levels, but not D1 Receptor, Alter Specifically Acute Responses to Psychostimulants

Corvol

Valjent

Pascoli

et al. 2006

Neuropsychopharmacol

View full text Add to dashboard Cite

Striatal dopamine D1 receptors (D1R) are coupled to adenylyl cyclase through Gaolf. Although this pathway is involved in important brain functions, the consequences of quantitative alterations of its components are not known. We explored the biochemical and behavioral responses to cocaine and D-amphetamine (D-amph) in mice with heterozygous mutations of genes encoding D1R and Gaolf (Drd1a + /À and Gnal + /À), which express decreased levels of the corresponding proteins in the striatum. Dopamine-stimulated cAMP production in vitro and phosphorylation of AMPA receptor GluR1 subunit in response to D-amph in vivo were decreased in Gnal + /À, but not Drd1a + /À mice. Acute locomotor responses to D1 agonist SKF81259, D-amph and cocaine were altered in Gnal + /À mice, and not in Drd1a + /À mice. This haploinsufficiency showed that Gaolf but not D1R protein levels are limiting for D1R-mediated biochemical and behavioral responses. Gnal + /À mice developed pronounced locomotor sensitization and conditioned locomotor responses after repeated injections of D-amph (2 mg/kg) or cocaine (20 mg/kg). They also developed normal D-amph-conditioned place preference. The D1R/cAMP pathway remained blunted in repeatedly treated Gnal + /À mice. In contrast, D-amph-induced ERK activation was normal in the striatum of these mice, possibly accounting for the normal development of long-lasting behavioral responses to psychostimulants. Our results clearly dissociate biochemical mechanisms involved in acute and delayed behavioral effects of psychostimulants. They identify striatal levels of Gaolf as a key factor for acute responses to psychostimulants and suggest that quantitative alterations of its expression may alter specific responses to drugs of abuse, or possibly other behavioral responses linked to dopamine function.

show abstract

Section: Gaolf and Not D1r Levels Control Acute Locomotor Effects Of mentioning

confidence: 41%

Section: Gaolf and Not D1r Levels Control Acute Locomotor Effects Of mentioning

confidence: 79%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Quantitative Changes in Gαolf Protein Levels, but not D1 Receptor, Alter Specifically Acute Responses to Psychostimulants

Corvol

Valjent

Pascoli

et al. 2006

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…However, the role of D1 receptors appears to vary depending on the type of psychostimulant administered and the process being studied, i.e., development versus expression. More specifically, the D1 receptor antagonist SCH 23390 blocks both the development and expression of amphetamine-induced and methamphetamine-induced behavioral sensitization Hamamura et al 1991;Kuribara and Uchihashi 1994;Kuribara 1995a;Vezina 1996;Karper et al 2002). In contrast, D1 receptor antagonism blocks the expression but it is not sufficient to prevent the development of cocaine-induced behavioral sensitization (Kuribara and Uchihashi 1993;Mattingly et al 1994;Kuribara 1995b;.…”

Section: Introductionmentioning

confidence: 88%

Studies on the role of dopamine D1 receptors in the development and expression of MDMA-induced behavioral sensitization in rats

2004

View full text Add to dashboard Cite

show abstract

“…However, the role of D1 receptors appears to vary depending on the psychostimulant and the process being studied, that is, development vs expression. More specifically, D1 receptor antagonist, SCH 23390 ((R)-( þ )-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride), blocks both the development and expression of amphetamine-and methamphetamineinduced behavioral sensitization Hamamura et al, 1991;Vezina, 1996;Karper et al, 2002). In contrast, D1 receptor antagonism blocks the expression but not the development of cocaine sensitization (Mattingly et al, 1994;.…”

Section: Introductionmentioning

confidence: 99%

Administration of SCH 23390 into the Medial Prefrontal Cortex Blocks the Expression of MDMA-Induced Behavioral Sensitization in Rats: An Effect Mediated by 5-HT2C Receptor Stimulation and not by D1 Receptor Blockade

Ramos

Goñi-Allo

Aguirre

2005

Neuropsychopharmacol

View full text Add to dashboard Cite

Akin to what has been reported for cocaine, systemic administration of the dopamine D1 receptor antagonist, SCH 23390 ((R)-( þ )-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride), blocks the expression but not the induction of 3,4-methylenedioxymethamphetamine (MDMA)-induced behavioral sensitization. Since the medial prefrontal cortex (mPFC) appears to regulate the expression of sensitization to cocaine, this study examined whether microinjection of SCH 23390 into the mPFC would alter the expression of MDMA sensitization. Saline or MDMA was administered for 5 consecutive days. After 12 days of withdrawal, rats received a bilateral intra-mPFC microinjection of SCH 23390 or saline followed by an intraperitoneal (i.p.) challenge dose of MDMA. While SCH 23390 enhanced locomotion in MDMA-naïve rats, it completely suppressed the expression of sensitization in MDMApretreated animals. Since, SCH 23390 has a fairly good affinity for 5-HT 2C receptors, we went further to study the role of mPFC D1 and 5-HT 2C receptors in this, apparently, paradoxical effect shown by SCH 23390. Thus, the microinjection of both SKF 81297 (R-( þ )-6-chloro-7,8-dihydroxy-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrobromide) and MK 212 (6-chloro-2-(1-piperazinyl)pyrazine hydrochloride), a D1 and 5-HT 2C receptor agonist, respectively, blocked MDMA sensitization. By contrast, the 5-HT 2C receptor antagonist, RS 102221 (8-[5-(2,4-dimethoxy-5-(4-trifluoromethylphenylsulfonamido)phenyl-5-oxopentyl]-1,3,8-triazaspiro [4,5]decane-2,4-dione hydrochloride), had no effect in MDMA-naïve or MDMA-sensitized animals, but reversed the effects of SCH 23390 in MDMApretreated rats. These results demonstrate that suppression of MDMA-induced sensitization by SCH 23390 is mediated by 5-HT 2C receptor stimulation in the mPFC and not by the blockade of mPFC D1 receptors. Furthermore, these data indicate that stimulation of 5-HT 2C receptors by SCH 23390 is not a minor issue and should be considered when interpreting future data.

show abstract

Role of D 1 -like receptors in amphetamine-induced behavioral sensitization: a study using D 1A receptor knockout mice

Cited by 40 publications

References 34 publications

Quantitative Changes in Gαolf Protein Levels, but not D1 Receptor, Alter Specifically Acute Responses to Psychostimulants

Quantitative Changes in Gαolf Protein Levels, but not D1 Receptor, Alter Specifically Acute Responses to Psychostimulants

Studies on the role of dopamine D1 receptors in the development and expression of MDMA-induced behavioral sensitization in rats

Administration of SCH 23390 into the Medial Prefrontal Cortex Blocks the Expression of MDMA-Induced Behavioral Sensitization in Rats: An Effect Mediated by 5-HT2C Receptor Stimulation and not by D1 Receptor Blockade

Contact Info

Product

Resources

About