ABSTRACT
The role of D1 and D2 striatal dopamine receptors on circling behavior was studied in a normosensitive model obtained by unilateral kainic acid lesion of the entopeduncular nucleus. In this model, the sensitivity of striatal dopamine receptors was preserved, because kainic acid destroyed the neurons of the entopeduncular nucleus and left undamage the fibers of passage and axon terminals. Systemic administration of SKF 38393 to these animals fails to induce circling activity. In contrast, administration of quinpirole elicited rotation toward the lesioned side, which was increased by concurrent injection of SKF 38393. This behavior was inhibited by pretreatment with either a specific D1 (SCH 23390) or D2 (-sulpiride) antagonist. The apomorphine also induced ipsilateral circling that was abolished by pretreatment with D1 or D2 antagonists. The above results suggest that coactivation of both D1 and D2 striatal dopamine receptors are necessary to induce rotation in this normosensitive model.
Subject(s)
Corpus Striatum/physiology , Receptors, Dopamine D1/drug effects , Receptors, Dopamine D2/drug effects , Stereotyped Behavior/drug effects , 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine/pharmacology , Animals , Apomorphine/pharmacology , Benzazepines/pharmacology , Corpus Striatum/anatomy & histology , Dopamine Agents/pharmacology , Dopamine D2 Receptor Antagonists , Dose-Response Relationship, Drug , Ergolines/pharmacology , Kainic Acid/pharmacology , Male , Quinpirole , Rats , Rats, Sprague-Dawley , Receptors, Dopamine D1/antagonists & inhibitors , Sulpiride/pharmacologyABSTRACT
The effect of repeated administration of haloperidol on the pancreatic secretion was studied in urethane-anesthetized Swiss mice. Haloperidol (2 mg/kg) injected daily i.p. for 7 days, increase the volume and protein content of the basal pancreatic juice significantly. This secretory activity was partially blocked by i.p. injection of atropine (5 mg/kg), both in control and treated animals. The volume of the secretory response to bethanechol, a cholinergic agonist, was decreased by haloperidol without any change in amylase release. From these findings it is concluded that repeated haloperidol treatment produces an increase of basal pancreatic secretion, which is probably the result of changes in the sensitivity of dopamine receptors of the gland.
