M V Ugrumov

Russian Academy of Sciences, Moskva, Moscow, Russia

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Publications (74)151.98 Total impact

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    ABSTRACT: We tested the hypothesis that brain-derived chemical stimuli contribute to direct endocrine regulation of peripheral organs during ontogeny before blood-brain barrier closure. Dopamine and gonadotropin-releasing hormone present in high concentration in peripheral blood only before blood-brain barrier closure were chosen as the chemical stimuli. It was shown than dopamine in concentrations equal to its level in the peripheral blood inhibits prolactin secretion in organotypic culture of the pituitary gland from newborn rats via specific receptors. Experiments on organotypic culture of neonatal rat testicles showed that gonadotropin-releasing hormone stimulates testosterone secretion via specific receptors. We proved that chemical stimuli entering common circulation from the brain before blood-brain barrier closure could exert direct endocrine effect on peripheral organs.
    Bulletin of Experimental Biology and Medicine 07/2015; DOI:10.1007/s10517-015-2945-2 · 0.37 Impact Factor
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    ABSTRACT: We studied the endocrine function of the noradrenergic system in the developing brain. The data on the age-related dynamics of the noradrenaline concentration in plasma and in the hypothalamus and mesencephalon-rhombencephalon before and after the formation of the blood-brain barrier indirectly indicates the possibility of noradrenaline secretion from the brain to the peripheral blood. The direct evidence that the rat brain may be a source of noradrenaline in the peripheral blood before the formation of the blood-brain barrier was first obtained using a model of chronic specific inhibition of noradrenaline synthesis in the neonatal rat brain. It suggests that the brain is involved in the regulation of the development and functioning of peripheral target organs during this period.
    Neurochemical Journal 04/2015; 9(2):95-100. DOI:10.1134/S1819712415020129 · 0.19 Impact Factor
  • Doklady Biological Sciences 01/2014; 454(1):5-8. DOI:10.1134/S0012496614010116
  • Journal of Electrocardiology 07/2013; 46(4):e5. DOI:10.1016/j.jelectrocard.2013.05.022 · 1.36 Impact Factor
  • Journal of Electrocardiology 07/2013; 46(4). DOI:10.1016/j.jelectrocard.2013.05.014 · 1.36 Impact Factor
  • Doklady Biological Sciences 09/2012; 446(1):286-9. DOI:10.1134/S0012496612050122
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    G R Khakimova · E A Kozina · A Ya Sapronova · M V Ugrumov
    Doklady Biological Sciences 10/2011; 440:284-6. DOI:10.1134/S0012496611050231
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    ABSTRACT: We tested our hypothesis that dopamine (DA) is secreted from the brain to the blood during the perinatal period of rat ontogeny when rats have no blood-brain barrier. We developed a specific pharmacological model to inhibit DA synthesis in the brain and maintain its constant level on the periphery using α-methyl-p-tyrosine (αMPT), an inhibitor of the key enzyme of DA synthesis tyrosine hydroxylase. On the basis of preliminary systemic administration of αMPT (200, 100, 80, and 50 μg), we selected a dose of the inhibitor of 50 μg, which excluded its effects on DA metabolism in peripheral organs. In subsequent experiments, αMPT was stereotaxically administered into the lateral brain ventricles of three-day-old rats at the selected dose. After this, we measured the concentration of catecholamines and metabolites using high performance liquid chromatography with electrochemical detection in the brain, Zuckerkandl’s organ, kidneys, adrenals, and plasma. We found that in 4 h after administration of the inhibitor, the DA concentration decreased in the brain by 54% and in the plasma by 74%, whereas in the peripheral organs it remained unchanged. Thus, we directly showed that DA is secreted from the brain in the general blood circulation before the formation of the BBB.
    Neurochemical Journal 09/2011; 5(3). DOI:10.1134/S1819712411030068 · 0.19 Impact Factor
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    ABSTRACT: Degeneration of dopaminergic (DAergic) neurons of the nigrostriatal system is the key stage in the pathogenesis of Parkinson's disease. The first symptoms of this disease are observed after degeneration of 70-80% neurons, which occurs over 20-30 years. The clinical stage of Parkinson's disease begins after this period. Late diagnostics of Parkinson's disease contributes to low efficiency of therapy for this disorder. Detailed study of the pathogenesis and development of preclinical diagnostic methods for Parkinson's disease are the urgent problems. This work was designed to develop a new experimental model of the preclinical and clinical stages of the disease. Experimental modeling was performed on C57Bl/6 mice using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). This agent is converted into the MPP(+)-neurotoxin in brain DAergic neurons. We showed that MPTP in a dose of 4 mg/kg has no effect on the nigrostriatal DAergic system. MPTP in a dose of 8-16 mg/kg produced the toxic effect only on DAergic axons, which simulates the preclinical stage of Parkinson's disease. MPTP in a dose of 20-40 mg/kg had the toxic effect on neuronal axons and bodies, which simulates the clinical stage of Parkinson's disease. The data suggest that progressive degeneration of DAergic neurons is accompanied by activation of compensatory mechanisms for functional deficiency of these cells.
    Bulletin of Experimental Biology and Medicine 03/2011; 150(5):566-9. DOI:10.1007/s10517-011-1191-5 · 0.37 Impact Factor
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    ABSTRACT: A degradation of the nigrostriatal dopaminergic (DA-ergic) system is the key component of pathogenesis of Parkinson's disease (PD). Initial clinical symptoms appear 20-30 years after the onset of neurodegeneration, at a 70% DA depletion in the striatum and a 50% loss of nigral DA-ergic neurons. Low efficacy of the therapy might be improved if preclinical diagnostics and preventive therapy are developed. The development of appropriate experimental models should precede clinical trials. This multidisciplinary study first managed to model in mice with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) all together the following stages of parkinsonism: (a) the early presymptomatic stage manifested by a subthreshold degeneration of axons and DA depletion in the striatum without loss of nigral cell bodies; (b) the advanced presymptomatic stage manifested by a subthreshold degeneration of striatal axons and DA depletion and by a subthreshold loss of nigral cell bodies; (c) the advanced presymptomatic stage characterized by threshold depletion of striatal DA and a loss of DA-ergic axons and nigral cell bodies resulting in motor dysfunction. The degeneration of axons proceeds and prevails that of cell bodies suggesting higher sensitivity to MPTP of the former. Compensatory processes were developed in parallel to neurodegeneration that was manifested by the increase of the DA content in individual nigral cell bodies and DA turnover in the striatum. The developed models might be exploited for: (a) an examination of pathogenetic mechanisms not only in the nigrostriatal system but also in other brain regions and in the periphery; (b) a study of the compensatory mechanisms under DA deficiency; (c) a search of precursors of motor disorders and peripheral biomarkers in presymptomatic parkinsonism; (d) the development of preventive therapy aiming to slow down the neurodegeneration and strengthen compensatory processes. Thus, the models of the early and advanced presymptomaic stages and of the early symptomatic stage of parkinsonism were developed in mice with MPTP.
    Neuroscience 03/2011; 181:175-88. DOI:10.1016/j.neuroscience.2011.03.007 · 3.33 Impact Factor
  • M A Abramova · A Calas · M Ugrumov
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    ABSTRACT: Osmotic stimulation (OS) of vasopressin (VP) neurons of the supraoptic nucleus (SON) promotes VP secretion and tyrosine hydroxylase (TH) expression in adult mammals. VP secretion is under a noradrenaline control, whereas the regulation of TH expression remains uncertain. This study was aimed to determine at what period of ontogenesis: (1) VP neurons begin to react to OS by modifying simultaneously VP and TH gene expression and synthesis, (2) the noradrenergic control of VP neurons is established. Rats on the 21st embryonic day (E), third postnatal day (P), P13 were salt loaded or salt loaded and treated with an antagonist (prazosin) or agonist (phenylephrine) of α1-adrenoreceptors. According to our immunocytochemical and in situ hybridization data, OS resulted in an increased amount of VP mRNA in each age group and of VP on E21 and P3. TH gene and synthesis was initially expressed under OS on P3. The number of TH-expressing neurons diminished by threefold in salt loaded rats from P3 to P13. OS combined with prazosin administration resulted in an increased level of VP mRNA on P3 and P13, but not on E21 suggesting the onset of the noradrenaline inhibitory control after birth. OS together with prazosin treatment stimulated TH expression on P3 and P13, whereas phenylephrine provided an opposite effect. Thus, VP neurons begin to react to OS by an increased VP synthesis at the end of fetal life and by the onset of TH expression shortly after birth; the expression of both substances appears to be under the inhibitory control of noradrenaline.
    Brain Structure and Function 01/2011; 215(3-4):195-207. DOI:10.1007/s00429-010-0290-9 · 4.57 Impact Factor
  • M V Ugrumov
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    ABSTRACT: The maintaining of homeostasis in the organism in response to a variable environment is provided by the highly hierarchic neuroendocrine-immune system. The crucial component of this system is the hypothalamus providing the endocrine regulation of key peripheral organs, and the adenohypophysis. In this case, neuron-derived signaling molecules (SM) are delivered to the blood vessels in hypothalamic "neurohaemal organs" lacking the blood-brain barrier (BBB), the posterior lobe of the pituitary and the median eminence. The release of SM to the blood vessels in most other brain regions is prohibited by BBB. According to the conventional concept, the development of the neuroendocrine system in ontogenesis begins with the "maturation" of peripheral endocrine glands which first are self-governed and then operate under the adenohypophysial control. Meantime, the brain maturation is under the control of SM secreted by endocrine glands of the developing organism and coming from the placenta and maternal organism. The hypothalamus is involved in the neuroendocrine regulation only after its full maturation that is followed by the conversion of the opened-looped neuroendocrine system to the closed-looped system as in adulthood. Neurons of the developing brain begin to secrete SM shortly after their origin and long before the establishment of specific interneuronal relations providing initially autocrine and paracrine morphogenetic influence on differentiating target neurons. Taking into account that the brain lacks BBB over this ontogenetic period, we hypothesized that it operates as the multipotent endocrine gland secreting SM to the general circulation and thereby providing the endocrine regulation of peripheral organs and the brain. The term "multipotent" means that the spectrum of the brain-derived circulating SM and their occupancy at the periphery in the developing organism should greatly exceed those in adulthood. In order to test this hypothesis, gonadotropin-releasing hormone (GnRH), dopamine (DA), and serotonin (5-hydroxytryptamine, 5-HT) were chosen as the markers of the presumptive endocrine function of the brain in ontogenesis. According to our data, the concentrations of GnRH, DA, and 5-HT in the rat general circulation during the perinatal period, i.e. before the establishment of BBB, was as high as those in the portal circulation in adulthood. The concentrations of circulating GnRH and DA dropped to almost undetectable level after the development of BBB suggesting their brain origin. This suggestion has been proven by showing an essential decrease of GnRH, DA, and 5-HT concentrations in general circulation of perinatal rats after microsurgical elimination of synthesizing neurons or the inhibition of specific syntheses in the brain before the establishment of BBB. GnRH, DA, and 5-HT apparently as dozens of other brain-derived SM appear to be capable of providing the endocrine influence on their peripheral targets like the adenohypophysis, gonads, kidney, heart, blood vessels, and the brain (endocrine autoregulation). Although the ontogenetic period of the brain operation as the multipotent endocrine gland is relatively short, the brain-derived SM are thought to be capable of providing long-lasting morphogenetic effects on peripheral targets and the brain. Thus, the developing brain operates as the multipotent endocrine gland from the onset of neurogenesis to the establishment of BBB providing the endocrine regulation of the developing organism.
    Neurochemical Research 02/2010; 35(6):837-50. DOI:10.1007/s11064-010-0127-1 · 2.55 Impact Factor
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    ABSTRACT: Hyperprolactinemia is neurodegenerative disease that develops in humans as a result of degeneration of dopaminergic (DA-ergic) neurons of the arcuate nucleus, which synthesize DA, a neurohormone inhibiting prolactin secretion by pituitary lactotropes. The design and detailed analysis of good experimental models of hyperprolactinemia may help us to understand the causes and mechanisms of the disease development and develop early diagnostics and treatment of the disease. Hyperprolactinemia is usually modeled in experiments using 6-hydroxydopamine (6-HDA), a neurotoxin causing degeneration of DA-ergic neurons of the arcuate nucleus. However, 6-HAD also induces degeneration of noradrenergic (NA-ergic) axons involved in the regulation of prolactin secretion. Therefore, in this study, we evaluated the role of NA in the development of hyperprolactinemia during degeneration of DA-ergic neurons of the arcuate nucleus. To this aim, we compared changes in DA and NA metabolism in the arcuate nucleus and the blood level of prolactin in rats after treatment with 6-HDA alone and 6-HDA in the presence of desmethylimipramine, drug that prevents degeneration of NA-ergic neurons. Studies were performed in 14 days after toxin administration, i.e., at a time point when toxin-induced degenerative processes are finished, and in 45 days, i.e., after initiation of compensatory processes. We found that, in 14 days after administration of pharmacological agents, hyperprolactinemia, which resulted from DA deficit due to degeneration of DA-ergic neurons of the arcuate nucleus, is enhanced when NA-ergic afferents are protected, which may be related to the inhibitory effect of NA on DA synthesis. The latter hypothesis is supported by the fact that in 45 days after treatment with 6-HDA alone, i.e., after combined degeneration of DA-ergic and NA-ergic neurons, DA synthesis in the arcuate nucleus returns back to the normal level, which is accompanied by recovery of the normal blood level of prolactin. In contrast, in 45 days after administration of 6-HDA and desmethylimipramine, NA synthesis increases to the normal level but DA synthesis in the arcuate nucleus remains at low level, which is accompanied by an increased blood level of prolactin. Thus, our data suggest that NA inhibits DA synthesis in the arcuate nucleus and prevents a compensatory increase in DA synthesis and the normalization of the blood level of prolactin during degeneration of DA-ergic neurons.
    Neurochemical Journal 12/2009; 3(4):288-296. DOI:10.1134/S1819712409040084 · 0.19 Impact Factor
  • M V Ugrumov
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    ABSTRACT: Besides the dopaminergic (DA-ergic) neurons possessing the whole set of enzymes of DA synthesis from l-tyrosine and the DA membrane transporter (DAT), the neurons partly expressing the DA-ergic phenotype have been first discovered two decades ago. Most of the neurons express individual enzymes of DA synthesis, tyrosine hydroxylase (TH) or aromatic l-amino acid decarboxylase (AADC) and lack the DAT. A list of the neurons partly expressing the DA-ergic phenotype is not restricted to so-called monoenzymatic neurons, e.g. it includes some neurons co-expressing both enzymes of DA synthesis but lacking the DAT. In contrast to true DA-ergic neurons, monoenzymatic neurons and bienzymatic non-dopaminergic neurons lack the vesicular monoamine transporter 2 (VMAT2) that raises a question about the mechanisms of storing and release of their final synthetic products. Monoenzymatic neurons are widely distributed all through the brain in adulthood being in some brain regions even more numerous than DA-ergic neurons. Individual enzymes of DA synthesis are expressed in these neurons continuously or transiently in norm or under certain physiological conditions. Monoenzymatic neurons, particularly those expressing TH, appear to be even more numerous and more widely distributed in the brain during ontogenesis than in adulthood. Most populations of monoenzymatic TH neurons decrease in number or even disappear by puberty. Functional significance of monoenzymatic neurons remained uncertain for a long time after their discovery. Nevertheless, it has been shown that most monoenzymatic TH neurons and AADC neurons are capable to produce l-3,4-dihydroxyphenylalanine (L-DOPA) from l-tyrosine and DA from L-DOPA, respectively. L-DOPA produced in monoenzymatic TH neurons is assumed to play a role of a neurotransmitter or neuromodulator acting on target neurons via catecholamine receptors. Moreover, according to our hypothesis L-DOPA released from monoenzymatic TH neurons is captured by monoenzymatic AADC neurons for DA synthesis. Such cooperative synthesis of DA is considered as a compensatory reaction under a failure of DA-ergic neurons, e.g. in neurodegenerative diseases like hyperprolactinemia and Parkinson's disease.Thus, a substantial number of the brain neurons express partly the DA-ergic phenotype, mostly individual complementary enzymes of DA synthesis, serving to produce DA in cooperation that is supposed to be a compensatory reaction under the failure of DA-ergic neurons.
    Journal of chemical neuroanatomy 09/2009; 38(4):241-56. DOI:10.1016/j.jchemneu.2009.08.004 · 2.52 Impact Factor
  • Doklady Biological Sciences 06/2009; 426:213-5. DOI:10.1134/S0012496609030065
  • Mikhail V Ugrumov
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    ABSTRACT: In contrast to monoaminergic (MA-ergic) neurons possessing the whole set of the enzymes for MA synthesis from the precursor amino-acid, some, mostly peptidergic, neurons co-express only one of the enzymes of monoamine synthesis. They are widely distributed in the brain, being particularly numerous in ontogenesis and, in adulthood, under certain physiological conditions. Most monoenzymatic neurons possess one of the enzymes for dopamine (DA) synthesis, tyrosine hydroxylase (TH) or aromatic L-amino acid decarboxylase (AADC). TH and AADC are enzymatically active in a substantial number of monoenzymatic neurons, where they are capable of converting L-tyrosine to L-3,4-dihydroxy-phenylalanine (L-DOPA) and L-DOPA to dopamine (DA) (or 5-hydroxy-tryptophan, 5-HTP to serotonin), respectively. According to our data L-DOPA synthesized in monoenzymatic TH-neurons is released and taken up by monoenzymatic AADC-neurons for DA synthesis. Moreover, L-DOPA captured by dopaminergic neurons and serotoninergic neurons serves to stimulate dopamine synthesis in the former and to start DA synthesis in the latter. Cooperative synthesis of MAs is considered as a compensatory reaction under a failure of MA-ergic neurons, e.g. in neurodegenerative diseases like hyperprolactinemia and Parkinson's disease, which are developed primarily because of degeneration of DA-ergic neurons of the tuberoinfundibular system and the nigrostriatal system, respectively. Noteworthy, the neurotoxin-induced increase of prolactin secretion returns with time to a normal level due to the stimulation of DA synthesis by the tuberoinfundibular most probably monoenzymatic neurons. The same compensatory mechanism is supposed to be used under the failure of the nigrostriatal DA-ergic system that is manifested by an increased number of monoenzymatic neurons in the striatum of animals with neurotoxin-induced parkinsonism and in humans with Parkinson's disease. Expression of the enzymes of MA synthesis in non-monoaminergic neurons is controlled by intercellular signals such as classical neurotransmitters (catecholamines), etc. Thus, a substantial number of brain neurons express partly the monoaminergic phenotype, namely individual complementary enzymes of MA synthesis, serving to produce MAs in cooperation, which is considered as a compensatory reaction under the failure of MA-ergic neurons.
    Journal de la Société de Biologie 02/2009; 203(1):75-85. DOI:10.1051/jbio:2009013
  • M Izvolskaia · A H Duittoz · Y Tillet · M V Ugrumov
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    ABSTRACT: Catecholamines (CA) play an important role in the regulation of GnRH neurons in adults, and it is probable that they control GnRH-neuron development. Migration of GnRH neurons was evaluated in male and female rats at the 17th embryonic day (E17) and E21, following the daily treatment of their pregnant mothers from the 11th to the 16th and 20th day of gestation with alpha-methyl-para-tyrosine (alphaMPT), an inhibitor of catecholamine synthesis. High-performance liquid chromatography with electrochemical detection (HPLC-ED) was used to specify the alphaMPT-induced CA depletion. There was a 50-70% decrease in dopamine and noradrenaline content in the nose and in the brain of alphaMPT-treated foetuses, proving the efficacy of this pharmacological model. Immunohistochemistry was used to evaluate the percentage (%) of GnRH neurons along their migration pathway from the vomeronasal organ (VNO) in the nose to the septo-preoptic area in the forebrain which is considered as an index of neuron migration. Special attention was paid to the topographic relationships of GnRH neurons with catecholaminergic fibres. These were observed in apposition with GnRH neurons in the entrance to the forebrain. In CA-deficient foetuses, the percentage of GnRH neurons located in the rostral regions extending from the VNO to the septum was greater than in controls. However, no statistically significant difference was found in the forebrain which extended from the septum to the retrochiasmatic area. In conclusion, these data suggest that endogenous catecholamines stimulate the GnRH neuron migration in ontogenesis.
    Brain Structure and Function 11/2008; 213(3):289-300. DOI:10.1007/s00429-008-0197-x · 4.57 Impact Factor
  • M. V. Ugrumov
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    ABSTRACT: In addition to the monoaminergic (MA-ergic) neurons possessing the whole set of enzymes of monoamine (MA) synthesis from the precursor amino acid and the MA membrane transporter, the neurons partly expressing the MA-ergic phenotype have been first discovered almost twenty years ago. Most of the neurons expressing individual enzymes of MA synthesis lack the MA transporter. These so-called monoenzymatic neurons are widely distributed throughout the brain in adult mammals being even more numerous than MA-ergic neurons. Individual enzymes of MA synthesis are expressed continuously or transiently over certain periods of ontogenesis and in adulthood under functional insufficiency of the MA-ergic neurons, e.g., under their chronic stimulation or in certain neurodegenerative diseases. The earlier data suggest an important functional role of monoenzymatic neurons. Most monoenzymatic neurons possess enzymes of dopamine (DA) synthesis, tyrosine hydroxylase (TH), or aromatic l-amino acid decarboxylase (AADC). TH and AADC are enzymatically active in a substantial number of monoenzymatic neurons being capable to convert l-tyrosine to l-3,4-dihydroxyphenylalanine (l-DOPA) and L-DOPA to DA or serotonin, respectively. L-DOPA produced in monoenzymatic TH-neurons is supposed to play a role of a neurotransmitter or a neuromodulator providing its action on the target neurons via catecholamine receptors. Moreover, l-DOPA released from the monoenzymatic TH-neurons is captured by monoenzymatic AADC-neurons or dopaminergic (DA-ergic) and serotoninergic neurons for DA synthesis (Kannari et al., 2006). Such cooperative synthesis of MAs is considered as a compensatory reaction under the failure of MA-ergic neurons, e.g., in neurodegenerative diseases like hyperprolactinemia and Parkinson's disease which are developed primarily because of the degeneration of DA-ergic neurons of the tuberoinfundibular system and the nigrostriatal system, respectively. Noteworthy, the neurotoxin-induced increased level of prolactin returns with time to the normal level due to stimulation of DA synthesis by the neurons of the tuberoinfundibular system, most probably because of the turning on cooperative synthesis of DA by monoenzymatic neurons. The same compensatory mechanism is supposed to be used under the failure of the nigrostriatal DA-ergic system that is manifested by the increased number of monoenzymatic neurons in the striatum of animals with neurotoxin-induced parkinsonism and in humans with Parkinson's disease. Expression of the enzymes of MA synthesis in non-MA-ergic neurons is controlled by intercellular signals such as classical neurotransmitters (catecholamines), neurotrophic factors (brain-derived neurotrophic factor, glia-derived neurotrophic factor), and perhaps hormones (prolactin, estrogens, progesterone). Thus, a substantial number of the brain neurons express partly the MA-ergic phenotype, mostly individual complementary enzymes of MA synthesis, serving to produce MAs in cooperation that is considered as a compensatory reaction under the failure of MA-ergic neurons.
    02/2008: pages 21-73;
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    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-HDA)—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, sections 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 sections 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 sections and incubation medium in experiments in vitro. 45 days after the neurotoxin administration, all the above parameters returned to the normal level. Thus, 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 arcuate nucleus. Key wordsdopamine–arcuate nucleus–6-hydroxydopamine–prolactine–rat
    Journal of Evolutionary Biochemistry and Physiology 01/2008; 44(1):82-88. DOI:10.1134/S0022093008010106 · 0.24 Impact Factor

Publication Stats

811 Citations
151.98 Total Impact Points

Institutions

  • 1979–2012
    • Russian Academy of Sciences
      • • Koltzov Institute of Developmental Biology
      • • Institute of Developmental Biology
      • • Laboratory of Hormonal Regulations
      Moskva, Moscow, Russia
  • 2000–2008
    • Russian Academy of Medical Sciences
      Moskva, Moscow, Russia
  • 2006
    • P.K. Anokhin Institute of Normal Physiology
      Московский, Moskovskaya, Russia
  • 2002
    • State University of New York Upstate Medical University
      • Department of Surgery
      Syracuse, New York, United States