title: [Compensatory reaction during degeneration of arcuate nucleus dopaminergic neurons in rats].
abstract: The study has been carried out to verify the authors' hypothesis that degeneration of dopaminergic (DA-ergic) neurons of the hypothalamic tuberoinfundibular system and concomitant development of hyperprolactinemia are accompanied by involvement of compensatory synthesis of dopamine (DA) by non-dopaminergic neurons expressing single complementary enzymes of synthesis of this neurotransmitter. Degeneration of DA-ergic neurons was produced by a stereotaxic injection into the brain lateral ventricles of 6-hydroxydopamine (6-OHDA) - a specific neurotoxin of DA-ergic neurons. 14 and 45 days after the toxin administration there were determined concentration of prolactine in peripheral blood by methods of immunoenzyme and radioimmunological analyses as well as the DA amount in the arcuate nucleus by the method of highly efficient liquid chromatography with electrochemical detection. In a part of the animals, slices were prepared from the mediobasal hypothalamus (arcuate nucleus and medial eminence) and perfused with Krebs-Ringer medium; then the DA concentration was determined in the slices and in the incubation medium. 14 days after the neurotoxin administration there were revealed an increase of blood prolactine concentration and a decrease of DA concentration in the arcuate nucleus in vivo as well a decrease of the total DA amount in the slices and incubation medium in experiments in vitro. 45 days after the neurotoxin administration, all the above parameters returned to the normal level. This, the obtained data indicate that the hyperlactinemia and DA deficit appearing during degeneration of the arcuate nucleus DA-ergic neurons seem to be compensated due to an enhancement of DA synthesis by non-dopaminergic monoenzyme neurons of arctuate nucleus.
authors.forename: G Z
authors.initials: GZ
authors.lastname: Ziiazetdinova
authors.forename: A Ia
authors.initials: AIa
authors.lastname: Sapronova
authors.forename: V Ia
authors.initials: VIa
authors.lastname: Kiiasova
authors.forename: A K
authors.initials: AK
authors.lastname: Nanaev
authors.forename: V S
authors.initials: VS
authors.lastname: Kudrin
authors.forename: N
authors.initials: N
authors.lastname: Martina
authors.forename: I
authors.initials: I
authors.lastname: Tyllet
authors.forename: M V
authors.initials: MV
authors.lastname: Ugriumov
mesh_terms: D018663:Adrenergic Agents / Q000633:toxicity; D000818:Animals; D001111:Arcuate Nucleus of Hypothalamus / Q000378:metabolism* / Q000473:pathology; D004298:Dopamine / Q000378:metabolism*; D008297:Male; D009410:Nerve Degeneration / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D009498:Neurotoxins / Q000633:toxicity; D016627:Oxidopamine / Q000633:toxicity; D011388:Prolactin / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D018663:Adrenergic Agents; D009498:Neurotoxins; D016627:Oxidopamine; D011388:Prolactin; D004298:Dopamine