title: Effects of a partial D2-like receptor agonist on striatal dopamine autoreceptor functioning in preweanling rats.
abstract: There is evidence that partial D2-like dopamine agonists (e.g., terguride) may not affect D2-like postsynaptic receptors in an adult-typical manner during the preweanling period. To determine whether synthesis modulating dopamine autoreceptors are also affected in an adult atypical manner by partial D2-like agonists, preweanling rats were treated either acutely or repeatedly with reserpine (low dopaminergic tone) or vehicle (high dopaminergic tone). The ability of terguride, quinpirole (a full D2-like agonist), or haloperidol (a D2-like antagonist) to alter striatal DOPA accumulation was assessed after NSD-1015 treatment on postnatal day (PD) 21. In a separate set of experiments, terguride's ability to modulate dopamine synthesis was assessed in rats treated with the nerve impulse flow inhibitor gamma-butyrolactone (GBL). Results showed that both terguride and quinpirole reduced striatal DOPA accumulation during a state of low dopaminergic tone (i.e., after reserpine pretreatment). During a state of high dopaminergic tone (i.e., after vehicle pretreatment), terguride had similar effects as haloperidol and increased DOPA accumulation. Terguride, like quinpirole, partially inhibited the GBL-induced increase in striatal DOPA accumulation. When considered together, these results indicate that synthesis modulating D2-like autoreceptors are functional during the late preweanling period, and they respond in an adult-typical manner to a partial D2-like agonist.
authors.affiliation: Department of Psychology, California State University, San Bernardino, CA 92407, USA.
authors.forename: Shelly T
authors.initials: ST
authors.lastname: Yoshida
authors.forename: Shelley A
authors.initials: SA
authors.lastname: Baella
authors.forename: Nancy M
authors.initials: NM
authors.lastname: Stuebner
authors.forename: Cynthia A
authors.initials: CA
authors.lastname: Crawford
authors.forename: Sanders A
authors.initials: SA
authors.lastname: McDougall
mesh_terms: D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D015107:4-Butyrolactone / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D017660:Autoreceptors / Q000502:physiology; D003342:Corpus Striatum / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism*; D018491:Dopamine Agonists / Q000494:pharmacology*; D018492:Dopamine Antagonists / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D004347:Drug Interactions; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006220:Haloperidol / Q000494:pharmacology; D006834:Hydrazines / Q000494:pharmacology; D008090:Lisuride / Q000031:analogs & derivatives* / Q000494:pharmacology; D019257:Quinpirole / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017448:Receptors, Dopamine D2 / Q000819:agonists; D012110:Reserpine / Q000008:administration & dosage
chemical_list: D017660:Autoreceptors; D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D004791:Enzyme Inhibitors; D006834:Hydrazines; D017448:Receptors, Dopamine D2; D015102:3,4-Dihydroxyphenylacetic Acid; D019257:Quinpirole; C006208:dironyl; D012110:Reserpine; C004297:3-hydroxybenzylhydrazine; D008090:Lisuride; D006220:Haloperidol; D015107:4-Butyrolactone; D004298:Dopamine