title: Behavioural deficits induced by an electrolytic lesion of the rat ventral mesencephalic tegmentum are corrected by a superimposed lesion of the dorsal noradrenergic system.
abstract: The bilateral electrolytic lesion of the ventral mesencephalic tegmentum (VMT) induces, in the rat, behavioural deficits such as locomotor hyperactivity and disappearance of spontaneous alternation ('VMT syndrome'). When a specific 6-hydroxy dopamine (6-OHDA) destruction of the dorsal noradrenergic (NA) ascending pathway was superimposed to an electrolytic lesion of the VMT, animals recovered a normal locomotor activity and the possibility to alternate. Since many studies indicate that the development of the 'VMT syndrome' is linked to the disruption of the dopaminergic (DA) meso-cortico-limbic transmission, it is proposed that the recovery observed is due to an interaction between NA and DA ascending systems in cortical and/or subcortical structures; noradrenergic innervation would have a permissive role on the expression of the 'VMT syndrome', possibly via a mechanism of heteroregulation of DA receptors by NA fibers.
mesh_terms: D000818:Animals; D002540:Cerebral Cortex / Q000502:physiology*; D004298:Dopamine / Q000032:analysis; D005106:Exploratory Behavior; D007839:Functional Laterality; D006892:Hydroxydopamines; D008297:Male; D009043:Motor Activity; D009638:Norepinephrine / Q000032:analysis; D009714:Nucleus Accumbens / Q000502:physiology*; D016627:Oxidopamine; D051381:Rats; D011919:Rats, Inbred Strains; D012686:Septal Nuclei / Q000502:physiology*; D013681:Tegmentum Mesencephali / Q000502:physiology*
chemical_list: D006892:Hydroxydopamines; D016627:Oxidopamine; D004298:Dopamine; D009638:Norepinephrine