title: Apomorphine-induced turning behavior in 6-hydroxydopamine lesioned rats is increased by histidine and decreased by histidine decarboxylase, histamine H1 and H2 receptor antagonists, and an H3 receptor agonist.
abstract: The role of histamine and its receptors in basal ganglia neurocircuitry was assessed in apomorphine-induced turning behavior. Rats with unilateral 6-hydroxydopamine lesions of the substantia nigra pars compacta and medial forebrain bundle were administered histaminergic agents, and apomorphine-induced turning behavior was tested on Days 7 and 14 post-lesion. Compared with saline-treated rats, histidine (500 mg/kg, i.p.), a precursor of histamine, increased turning behavior (p<0.05), while alpha-fluoromethylhistidine (alpha-FMH, 25 microg, i.c.v.), an irreversible inhibitor of histidine decarboxylase, decreased turning behavior (p<0.05) but only on Day 14 post-lesion. Both the histamine H(1) receptor antagonist pyrilamine (10 and 50 microg, i.c.v.) and the H(2) receptor antagonist cimetidine (10 and 50 microg, i.c.v.) significantly decreased turning behavior on Days 7 and 14 post-lesion. The histamine H(3) receptor agonist immepip (10 microg, i.c.v.) decreased turning behavior (p<0.05) on Day 14 post-lesion. The present findings indicate the complex interactions of histamine on basal ganglia function.
authors.affiliation: Department of Neurobiology, Institute of Neuroscience, Zhejiang University, School of Medicine, Hangzhou, 310058, China.
authors.forename: Chun-Qing
authors.initials: CQ
authors.lastname: Liu
authors.forename: Dan-Na
authors.initials: DN
authors.lastname: Hu
authors.forename: Fu-Xin
authors.initials: FX
authors.lastname: Liu
authors.forename: Zhong
authors.initials: Z
authors.lastname: Chen
authors.forename: Jian-Hong
authors.initials: JH
authors.lastname: Luo
mesh_terms: D000818:Animals; D001058:Apomorphine / Q000494:pharmacology*; D001479:Basal Ganglia / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000008:administration & dosage / Q000494:pharmacology; D017442:Histamine Agonists / Q000494:pharmacology*; D006634:Histamine H1 Antagonists / Q000494:pharmacology*; D006635:Histamine H2 Antagonists / Q000494:pharmacology*; D006639:Histidine / Q000494:pharmacology; D006640:Histidine Decarboxylase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D007093:Imidazoles / Q000494:pharmacology; D007276:Injections, Intraventricular; D008297:Male; D008762:Methylhistidines / Q000008:administration & dosage / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology*; D016627:Oxidopamine / Q000633:toxicity*; D010880:Piperidines / Q000494:pharmacology; D011738:Pyrilamine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013239:Stereotyped Behavior / Q000187:drug effects*; D013565:Sympatholytics / Q000633:toxicity*; D013569:Synapses / Q000187:drug effects; D013890:Thiourea / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D017442:Histamine Agonists; D006634:Histamine H1 Antagonists; D006635:Histamine H2 Antagonists; D007093:Imidazoles; D008762:Methylhistidines; D009292:Narcotic Antagonists; D010880:Piperidines; D013565:Sympatholytics; C085755:4-(1H-imidazol-4-ylmethyl)piperidine; D006639:Histidine; C028309:alpha-fluoromethylhistidine; D016627:Oxidopamine; D006640:Histidine Decarboxylase; D013890:Thiourea; D011738:Pyrilamine; D001058:Apomorphine; C086108:clobenpropit