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Titolo:
Modulation of histamine H-3 receptors in the brain of 6-hydroxydopamine-lesioned rats
Autore:
Anichtchik, OV; Huotari, M; Peitsaro, N; Haycock, JW; Mannisto, PT; Panula, P;
Indirizzi:
Abo Akad Univ, Dept Biol, Turku 20520, Finland Abo Akad Univ Turku Finland 20520 Univ, Dept Biol, Turku 20520, Finland Grad Sch Biomed Sci TuBS, Turku, Finland Grad Sch Biomed Sci TuBS Turku Finland Biomed Sci TuBS, Turku, Finland Univ Kuopio, Dept Pharmacol & Toxicol, FIN-70211 Kuopio, Finland Univ Kuopio Kuopio Finland FIN-70211 Toxicol, FIN-70211 Kuopio, Finland Univ Kuopio, Grad Sch Pharm, FIN-70211 Kuopio, Finland Univ Kuopio Kuopio Finland FIN-70211 ch Pharm, FIN-70211 Kuopio, Finland Louisiana State Univ, Med Ctr, Dept Biochem & Mol Biol, New Orleans, LA USA Louisiana State Univ New Orleans LA USA & Mol Biol, New Orleans, LA USA Univ Helsinki, Dept Anat, Inst Biomed, FIN-00014 Helsinki, Finland Univ Helsinki Helsinki Finland FIN-00014 ed, FIN-00014 Helsinki, Finland
Titolo Testata:
EUROPEAN JOURNAL OF NEUROSCIENCE
fascicolo: 11, volume: 12, anno: 2000,
pagine: 3823 - 3832
SICI:
0953-816X(200011)12:11<3823:MOHHRI>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
DECARBOXYLASE MESSENGER-RNA; GLUTAMIC-ACID DECARBOXYLASE; PARKINSONS-DISEASE; SUBSTANTIA-NIGRA; DOPAMINERGIC-NEURONS; GABA RELEASE; HISTIDINE-DECARBOXYLASE; INCREASED EXPRESSION; STRIATAL DOPAMINE; BASAL GANGLIA;
Keywords:
GTP-gamma-[S-35] autoradiography; H-3 receptor binding; immunohistochemistry; Parkinson's disease;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Panula, P Abo Akad Univ, Dept Biol, BioCity,Artillerigatan 6, Turku 20520,Finland Abo Akad Univ BioCity,Artillerigatan 6 Turku Finland 20520 land
Citazione:
O.V. Anichtchik et al., "Modulation of histamine H-3 receptors in the brain of 6-hydroxydopamine-lesioned rats", EUR J NEURO, 12(11), 2000, pp. 3823-3832

Abstract

Parkinson's disease is a major neurological disorder that primarily affects the nigral dopaminergic cells. Nigral histamine innervation is altered inhuman postmortem Parkinson's disease brains. However, it is not known if the altered innervation is a consequence of dopamine deficiency. The aim of the present study was to investigate possible changes in the H-3 receptor system in a well-characterized model of Parkinson's disease - the 6-hydroxydopamine (6-OHDA) lesioned rats. Histamine immunohistochemistry showed a minor increase of the fibre density index but we did not find any robust increase of histaminergic innervation in the ipsilateral substantia nigra on thelesioned side. In situ hybridization showed equal histidine decarboxylase mRNA expression on both sides in the posterior hypothalamus. H-3 receptors were labelled with N-alpha-[3H]-methyl histamine dihydrochloride ([H-3] NAMH). Upregulation of binding to H-3 receptors was found in the substantia nigra and ventral aspects of striatum on the ipsilateral side. An increase ofGTP-gamma-[S-35] binding after H-3 agonist activation was found in the striatum and substantia nigra on the lesioned side. In situ hybridization of H-3 receptor mRNA demonstrated region-specific mRNA expression and an increase of H-3 receptor mRNA in ipsilateral striatum. Thus, the histaminergic system is involved in the pathological process after 6-OHDA lesion of the ratbrain at least through H-3 receptor. On the later stages of the neurotoxicdamage, less H-3 receptors became functionally active. Increased H-3 receptor mRNA expression and binding may, for example, modulate GABAergic neuronal activity in dopamine-depleted striatum.

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Documento generato il 25/01/20 alle ore 09:31:10