title: Suppression of noradrenergic innervation compensates for behavioral deficits induced by lesion of dopaminergic terminals in the lateral septum.
abstract: Spontaneous alternation which is disrupted by lesion of septal dopaminergic (DA) afferents was chosen as a behavioral marker for the study of functional interactions between DA and noradrenergic (NA) innervation of the lateral septum. Three groups of rats were studied: a solvent group which received only vehicle injection, and two lesioned groups, one with DA lesion and the second with simultaneous DA + NA lesion of the septal innervation. DA lesion was produced by infusing 6-hydroxydopamine (6-OHDA) into the lateral septum after pretreatment with desmethylimipramine (DMI) injected intraperitoneally. The DA + NA lesion was produced by infusing 6-OHDA without DMI pretreatment. The lesion of DA innervation alone led to a disturbance of alternation behavior in a Y-maze, but performance was not affected by the combined DA + NA lesion. The group with septal DA lesion was then injected with 6-OHDA into the pedunculus cerebellaris superior (PCS) in order to destroy NA efferents from the locus coeruleus. The two other groups were sham-operated. After post-operative recovery, the rats were retested for spontaneous alternation. The rats with the PCS NA lesion subsequent to the DA septal lesion displayed normal alternation behavior. Their performance was not different from that of animals with both NA and DA lesions in the septum. Thus the NA lesion appears to prevent the alternation deficits induced by the DA septal lesion, and also abolishes the deficits induced by the prior DA lesions. These results may have therapeutic implications.
authors.affiliation: Laboratoire de Psychobiologie des Comportements Adaptatifs, I.N.S.E.R.M. U-259, Université de Bordeaux II, France.
authors.forename: K
authors.initials: K
authors.lastname: Taghzouti
authors.forename: M
authors.initials: M
authors.lastname: Le Moal
authors.forename: H
authors.initials: H
authors.lastname: Simon
mesh_terms: D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000818:Animals; D002531:Cerebellum / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D002540:Cerebral Cortex / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D003891:Desipramine / Q000494:pharmacology*; D004298:Dopamine / Q000378:metabolism / Q000502:physiology*; D004525:Efferent Pathways / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D006897:Hydroxyindoleacetic Acid / Q000378:metabolism; D007858:Learning / Q000187:drug effects / Q000502:physiology*; D008125:Locus Coeruleus / Q000502:physiology*; D008297:Male; D009638:Norepinephrine / Q000378:metabolism / Q000502:physiology*; D009714:Nucleus Accumbens / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D016627:Oxidopamine / Q000633:toxicity*; D051381:Rats; D011919:Rats, Inbred Strains; D012016:Reference Values; D012688:Septum Pellucidum / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D012701:Serotonin / Q000378:metabolism
chemical_list: D015102:3,4-Dihydroxyphenylacetic Acid; D012701:Serotonin; D006897:Hydroxyindoleacetic Acid; D016627:Oxidopamine; D003891:Desipramine; D004298:Dopamine; D009638:Norepinephrine