title: Ontogenetic quinpirole treatment produces long-lasting decreases in the expression of Rgs9, but increases Rgs17 in the striatum, nucleus accumbens and frontal cortex.
abstract: Ontogenetic treatment of rats with the dopamine D(2)-like receptor agonist quinpirole produces a significant increase in dopamine D(2) receptor sensitivity that persists throughout the animal's lifetime, a phenomenon known as D(2) priming. The present study was designed to investigate the effects of priming of the D(2) receptor on the expression of three different members of the regulator of G-protein signaling (RGS) family: Rgs4, Rgs9 and Rgs17. Male offspring were ontogenetically treated with quinpirole or saline from postnatal days (P)1-21 and raised to adulthood. On approximately P65, animals were given an acute quinipirole injection (0.1 mg/kg) and the number of yawns was recorded for 1 h after the injection. Yawning has been shown to be a behavioural event mediated by the dopamine D(2)/D(3) receptor. Animals ontogenetically treated with quinpirole demonstrated a significant 2.5-fold increase in yawning as compared to controls. Rgs transcripts were analysed through in situ hybridization several weeks later. Rats ontogenetically treated with quinpirole demonstrated a significant decrease in Rgs9 expression in the frontal cortex, but a more robust decrease in the striatum and nucleus accumbens as compared to controls. Regarding Rgs17, ontogenetic quinpirole produced a modest but significant increase in expression in the same brain areas. There were no significant differences in Rgs4 expression produced by drug treatment in any of the brain regions analysed. This study demonstrates that ontogenetic quinpirole treatment, which results in priming of the D(2) receptor, results in significant decreases in Rgs9, which has been shown to regulate G-protein coupling to D(2) receptors.
authors.affiliation: Department of Psychology, East Tennessee State University, Johnson City, TN 37614, USA.
authors.forename: Amanda M
authors.initials: AM
authors.lastname: Maple
authors.forename: Marla K
authors.initials: MK
authors.lastname: Perna
authors.forename: Joshua P
authors.initials: JP
authors.lastname: Parlaman
authors.forename: Gregg D
authors.initials: GD
authors.lastname: Stanwood
authors.forename: Russell W
authors.initials: RW
authors.lastname: Brown
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism; D003342:Corpus Striatum / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism; D018491:Dopamine Agonists / Q000494:pharmacology; D005260:Female; D005625:Frontal Lobe / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism; D019204:GTP-Binding Proteins / Q000187:drug effects / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects* / Q000502:physiology; D008297:Male; D009714:Nucleus Accumbens / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism; D019257:Quinpirole / Q000494:pharmacology*; D020710:RGS Proteins / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017448:Receptors, Dopamine D2 / Q000187:drug effects* / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000187:drug effects / Q000378:metabolism; D013995:Time; D015000:Yawning / Q000187:drug effects / Q000502:physiology
chemical_list: D018491:Dopamine Agonists; D020710:RGS Proteins; C491349:RGS5 protein, human; D017448:Receptors, Dopamine D2; D043562:Receptors, G-Protein-Coupled; C527168:Rgs17 protein, rat; C116925:regulator of g-protein signaling 9; D019257:Quinpirole; D019204:GTP-Binding Proteins; D004298:Dopamine