title: Regulation of neurotensin-containing neurons in the rat striatum. Effects of unilateral striatal lesions with quinolinic acid and ibotenic acid on neurotensin content and its binding site density.
abstract: Recently, we reported bilateral increases in striatal neurotensin (NT) levels following unilateral 6-hydroxydopamine lesion of the nigrostriatal dopaminergic pathway. In the present study, the effect of unilateral striatal lesions with quinolinic acid (QA, 300 nmol) or ibotenic acid (IBO, 130 nmol) on striatal NT levels and binding site densities were analyzed in order to investigate other possible regulations of NT systems. QA and IBO injection decreased gamma-aminobutyric acid (GABA) levels and [125I]iodosulpride (a specific D2 receptor antagonist) binding site densities in the lesioned striatum, indicating degeneration of striatal intrinsic neurons. Striatal dopaminergic terminals were not altered by QA as shown by the lack of changes in [3H]dihydrotetrabenazine [( 3H]TBZOH, a specific ligand of the vesicular monoamine transporter) binding site densities. Moreover, QA lesion induced an increase in NT levels and a decrease in NT binding sites in the lesioned striatum without any change in the contralateral structure. In contrast to QA, IBO might destroy a certain proportion of dopaminergic terminals in the lesioned striatum, as shown by a 54% decrease in [3H]TBZOH binding. Furthermore, IBO lesion enhanced striatal NT levels bilaterally, while NT binding sites decreased in the lesioned striatum and increased in the contralateral side. The present results suggest that not only dopaminergic neurons but also striatal intrinsic neurons may control NT systems in the striatum.
authors.affiliation: INSERM U.55, Hôpital Saint-Antoine, Paris, France.
authors.forename: Y
authors.initials: Y
authors.lastname: Masuo
authors.forename: M N
authors.initials: MN
authors.lastname: Montagne
authors.forename: D
authors.initials: D
authors.lastname: Pélaprat
authors.forename: D
authors.initials: D
authors.lastname: Scherman
authors.forename: W
authors.initials: W
authors.lastname: Rostène
mesh_terms: D000818:Animals; D001665:Binding Sites; D001679:Biogenic Amines / Q000378:metabolism; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D007839:Functional Laterality; D007051:Ibotenic Acid / Q000633:toxicity*; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D009496:Neurotensin / Q000378:metabolism*; D017378:Quinolinic Acid; D011805:Quinolinic Acids / Q000633:toxicity*; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000378:metabolism; D017448:Receptors, Dopamine D2; D018028:Receptors, Neurotensin; D017981:Receptors, Neurotransmitter / Q000378:metabolism*; D012016:Reference Values; D013238:Stereotaxic Techniques; D013469:Sulpiride / Q000031:analogs & derivatives / Q000378:metabolism; D013747:Tetrabenazine / Q000031:analogs & derivatives / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D001679:Biogenic Amines; D011805:Quinolinic Acids; D011954:Receptors, Dopamine; D017448:Receptors, Dopamine D2; D018028:Receptors, Neurotensin; D017981:Receptors, Neurotransmitter; C045105:iodosulpride; D007051:Ibotenic Acid; C032811:dihydrotetrabenazine; D009496:Neurotensin; D005680:gamma-Aminobutyric Acid; D013469:Sulpiride; D017378:Quinolinic Acid; D013747:Tetrabenazine