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Experimental Brain Research

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01.03.2007 | Research Article

Nicotinamide prevents the effect of perinatal asphyxia on dopamine release evaluated with in vivo microdialysis 3 months after birth

verfasst von: Diego Bustamante, Paola Morales, Jorge Torres Pereyra, Michel Goiny, Mario Herrera-Marschitz

Erschienen in: Experimental Brain Research | Ausgabe 3/2007

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Abstract

The present study shows that nicotinamide prevents the long-term effect of perinatal asphyxia on dopamine release monitored with in vivo microdialysis in the neostriatum of 3-month-old rats. Perinatal asphyxia was induced by immersing foetuses-containing uterine horns removed from ready-to-deliver rats into a water bath for 16 or 20 min. Sibling, spontaneous, and caesarean-delivered pups were used as controls. Saline or nicotinamide (0.8 mmol/kg, i.p.) was administered to control and asphyxia-exposed animals 24, 48, and 72 h after birth. After weaning, the rats were randomly distributed in laboratory cages for animal care under standard ad libitum laboratory conditions. Approximately 3 months after birth, control and asphyxia-exposed animals were implanted with microdialysis probes into the lateral neostriatum for measuring extracellular monoamine and metabolite levels with HPLC-coupled to an electrochemical detection system under basal, D-amphetamine, and K⁺-depolarising conditions. There was an asphyxia-dependent decrease of extracellular dopamine levels, mainly observed during the periods when D-amphetamine (100 μM) or KCl (100 mM) was added into the perfusion medium. Compared to that observed in caesarean-delivered controls, the effect of D-amphetamine on dopamine levels was decreased by approximately 30 and 70% in animals exposed to 16 and 20 min of perinatal asphyxia, respectively. The effect of K⁺-depolarisation was decreased by 45 and 83% in animals exposed to the same periods of asphyxia, respectively. Both effects were prevented by nicotinamide, even if the treatment started 24 h after the insult. The present results support the idea of nicotinamide as an interesting molecule, useful for protecting against anoxia/ischemia occurring at neonatal stages. Nicotinamide can help to restore NADH/NAD⁺ depletion, but also to inhibit PARP-1 overactivation, a mechanism of action that has attracted attention, representing a novel target for neuroprotection following insults involving energy failure.

Amé J-C, Spenlehauer C, de Murcia G (2004) The PARP superfamily. BioEssays 26:882–893PubMedCrossRef

Abdelkarim GE, Gertz K, Harms C, Katchanov J, Dimagl U, Szabo C, Endres M (2001) Protective effects of PJ34, a novel, potent inhibitor of poly(ADP-ribose) polymerase (PARP) in vitro and in vivo models of stroke. Int J Mol Med 7:255–260PubMed

Akhter W, Ashraf QM, Zanelli SA, Mishra OP, Delivoria-Papadopoulus M (2001) Effect of graded hypoxia on cerebral cortical genomic DNA fragmentation in newborn piglets. Biol Neonate 79:187–193PubMedCrossRef

Andersson K, Blum M, Chen Y, Eneroth P, Gross J, Herrera-Marschitz M, Bjelke B, Bolme P, Diaz R, Jamison L, Loidl F, Ungethüm U, Åström G, Ögren SÖ (1995) Perinatal asphyxia increases bFGF mRNA levels and DA cell body number in mesencephalon of rats. NeuroReport 6:375–378PubMedCrossRef

Barkovich AJ (2006) MR imaging of the neonatal brain. Neuroimaging Clin N Am 16:117–135PubMedCrossRef

Berger NA (1985) Poly (ADP-ribose) in the cellular response to DNA damage. Radiat Res 1001:4–15CrossRef

Berger R, Garnier Y (2000) Perinatal brain injury. J Perinat Med 28:261–285PubMedCrossRef

Boksa P, El Khodor BP (2003) Birth insult interacts with stress at adulthood to alter dopaminergic function in animal models: possible implications for schizophrenia and other disordes. Neurosci Biobehav Rev 27:91–101PubMedCrossRef

Bustamante D, Zhi-Bing Y, Castel MN, Johansson S, Goiny M, Terenius L, Hökfelt T, Herrera-Marschitz M (2002) Effect of repeated methamphetamine treatment on neurotransmiter release in substantia nigra and neostriatum of the rat. J Neurochem 83:645–654PubMedCrossRef

Bustamante D, Goiny M, Åström G, Gross J, Andersson K, Herrera-Marschitz M (2003) Nicotinamide prevents the long-term effects of perinatal asphyxia on basal ganglia monoamine systems in the rat. Exp Brain Res 148:227–232PubMed

Butcher SP, Fairbrother IS, Kelly JS, Arbuthnott GW (1988) Amphetamine-induced release in the rat striatum: an in vivo microdialysis study. J Neurochem 50:346–355PubMedCrossRef

Calabresi P, Centonze D, Bernardi G (2000) Cellular factors controlling neuronal vulnerability in the brain: a lesson from the striatum. Neurology 55:1249–1255PubMed

Carter BS, Haverkamp AD, Merenstein GB (1993) The definition of acute perinatal asphyxia. Clin Perinatol 20:287–303PubMed

Chen Y, Ögren SÖ, Bjelke B, Bolme P, Eneroth P, Gross J, Loidl F, Herrera-Marschitz M, Andersson K (1995) Nicotine treatment counteracts perinatal-induced changes in the mesostriatal/limbic dopamine systems and in motor behaviour in the four-week-male rat. Neuroscience 68:531–538PubMedCrossRef

Chen Y, Herrera-Marschitz M, Bjelke B, Blum M, Gross J, Andersson K (1997a) Perinatal asphyxia-induced changes in rat brain tyrosine-hydroxylase-immunoreactive cell body number: effects of nicotine treatment. Neurosci Lett 221:77–80CrossRef

Chen Y, Hillefors-Berglund M, Herrera-Marschitz M, Bjelke B, Gross J, Andersson K, von Euler G (1997b) Perinatal asphyxia induces long-term changes in dopamine D1, D2 and D3 receptor binding in the rat brain. Exp Neurol 146:74–80CrossRef

Chen Y, Engidawork E, Loidl F, Dell’Anna E, Goiny M, Lubec G, Andersson K, Herrera-Marschitz M (1997c) Short- and long-term effects of perinatal asphyxia on monoamine, amino acid and glycolysis product levels measured in the basal ganglia of the rat. Dev Brain Res 104:19–30CrossRef

Cowan F, Rutherford M, Groenendaal F, Eken P, Mercuri E, Bydder GM, Meiners LC, Dubowitz LMS, de Vries LS (2003) Origin and timing of brain lesions in term infants with neonatal encephalopathy. Lancet 361:736–742PubMedCrossRef

Dell’Anna E, Chen Y, Engidawork E, Andersson K, Lubec G, Luthman J, Herrera-Marschitz M (1995) Short-term effects of perinatal asphyxia studied with Fos-inmunocytochemistry and in vivo microdialysis in the rat. Exp Neurol 131:279–287PubMedCrossRef

Dell’Anna E, Chen Y, Engidawork E, Andersson K, Lubec G, Luthman J, Herrera-Marschitz M (1997) Delayed neuronal death following perinatal asphyxia in rat. Exp Brain Res 115:105–115PubMedCrossRef

De Murcia G, Schreiber V, Molinete M, Saulier B, Poch O, Masson M, Niedergang C, Menesier de Murcia J (1994) Structure and function of poly(ADP-ribose) polymerase. Mol Cell Biochem 138:15–24PubMedCrossRef

Ducrocq S, Benjelloun N, Plotkine M, Ben-Ari Y, Charriaut-Marlangue C (2000) Poly(ADP-ribose) synthase inhibition reduces ischemic injury and inflammation in neonatal rat brain. J Neurochem 74:2504–2511PubMedCrossRef

Eliasson MJ, Sampei K, Madier AS, Hurn PD, Traystman RJ, Bao J, Pieper A, Wang ZQ, Dawson TM, Snyder SH (1997) Poly(ADP-ribose) Polymerase gene disruption renders mice resistant to cerebral ischemia. Nat Med 3:1089–1095PubMedCrossRef

Engidawork E, Loidl F, Chen Y, Kohlhauser C, Stoeckler S, Dell’Anna, Lubec G, Goiny M, Gross J, Andersson K, Herrera-Marschitz M (2001) Comparison between hypothermia and glutamate antagonism treatments on the immediate outcome of perinatal asphyxia. Exp Brain Res 138:375–383PubMedCrossRef

Gluckman PD, Wyatt JS, Azzopardi D, Ballard R, Edwards AD, Ferreiro DM, Polin RA, Robertson CM, Thoresen M, Whitelaw A, Gunn AJ (2005) Selective head cooling with mild systemic hypothermia after neonatal encephalopathy: multicenter randomised trial. Lancet 365:663–670PubMed

Gross J, Müller I, Chen Y, Elizade M, Leclere N, Herrera-Marschitz M, Andersson K (2000) Perinatal asphyxia induces region-specific long-term changes in mRNA levels of tyrosine hydroxylase and dopamine D1 and D2 receptors in rat brain. Brain Res Mol Brain Res 79:110–117PubMedCrossRef

Gross J, Andersson K, Chen Y, Müller I, Andreeva N, Herrera-Marschitz M (2005) Effect of perinatal asphyxia on tyrosine hydroxylase and D2 and D1 dopamine receptor mRNA levels expressed during early postnatal development in rat brain. Mol Brain Res 134:275–281PubMedCrossRef

Gunn AJ, Cook CJ, Williams CE, Johnston BM, Gluckman PD (1991) Electrophysiological responses of the fetus to hypoxia and asphyxia. J Dev Physiol 16:147–153PubMed

Gunn AJ, Thoressen M (2006) Hypothermic neuroprotection. NeuroRx 3:154–169PubMedCrossRef

Haddad GG, Jiang C (1993) O₂ deprivation in the central nervous system: on the mechanisms of neuronal response, differential sensitivity and injury. Prog Neurobiol 40:277–318PubMedCrossRef

Herrera-Marschitz M, Meana JJ, O’Connor WT, Goiny M, Reid MS, Ungerstedt U (1992) Neuronal dependence of extracellular, dopamine, acetylcholine, glutamate, aspartate and gamma-aminobutyric acid (GABA) measured simultaneously from rat neostriatum using in vivo microdialysis: reciprocal interactions. Amino Acids 2:157–179CrossRef

Herrera-Marschitz M, Loidl CF, Andersson K, Silveira R, O’Connor WT, Goiny M (1994) Neurocircuitry of the basal ganglia studied by monitoring neurotransmitter release: effects of intracerebral and perinatal lesions. Mol Neurobiol 9:171–182PubMed

Herrera-Marschitz M, You Z-B, Goiny M, Meana JJ, Silveira R, Godukhin O, Chen Y, Espinoza S, Pettersson E, Loidl F, Lubec G, Andersson K, Nylander I, Terenius L, Ungerstedt U (1996) On the origin of extracellular glutamate levels monitored in the basal ganglia by in vivo microdialysis. J Neurochem 66:1726–1735PubMedCrossRef

Hong SJ, Dawson TM, Dawson VL (2004) Nuclear and mitochondrial conversations in cell death: PARP-1 and AIF signalling. TIPS 25:259–264PubMed

Hurd J, Ungerstedt U (1989) Calcium dependency of amphetamine, nomifensine and Lu 19-005 effects on dopamine transmission. Eur J Pharmacol 166:261–270PubMedCrossRef

Iwashita A, Tojo N, Matsuura S, Yamazaki S, Kamijo K, Ishida J, Yamamoto H, Hattori K, Matsuoka N, Mutoh S (2004) A novel and potent Poly(ADP-Ribose) Polymerase-1 inhibitor, FR247304 (5-chloro-2-[3-(4-phenyl-3,6-dihydro-1(2H0-pyridinyl)propyl]-4(3H)-quinazolinone) attenuates neuronal damage in vitro and in vivo models of cerebral ischemia. J Pharmacol Exp Ther 310:425–436PubMedCrossRef

Jiang B-H, Rue E, Wang GL, Roe R, Semenza GL (1996) Dimerization, DNA binding, and transactivation properties of hypoxia-inducible factor 1. J Biol Chem 271:17771–17778PubMedCrossRef

Kamanaka Y, Kondo K, Ikeda Y, Kamoshima W, Kitajima T, Suzuki Y, Nakamura Y, Umemura K (2004) Neuroprotective effects of ONO-1924H, an inhibitor of poly ADP-ribose polymerase (PARP), on cytotoxicity of PC12 cells and ischemic cerebral damage. Life Sci 76:151–162PubMedCrossRef

Kihara S, Shiraishi T, Nakagawa S, Toda K, Tabuchi K (1994) Visualization of DNA double strand breaks in the gerbil hippocampal CA1 following transient ischemia. Neurosci Lett 175:133–136PubMedCrossRef

Klawitter V, Morales P, Johansson S, Bustamante D, Goiny M, Gross J, Luthman J, Herrera-Marschitz (2005) Effect of perinatal asphyxia on cell survival, neuronal phenotype and neurite growth evaluated with organotypic triple cultures. Amino Acids 28:149–155PubMedCrossRef

Kohlhauser C, Mosgoeller W, Hoeger H, Lubec G, Lubec B (1999a) Cholinergic, monoaminergic and glutamatergic changes following perinatal asphyxia in the rat. Cell Mol Life Sci 55:1491–1501CrossRef

Kohlhauser C, Kaehler S, Mosgoeller W, Singewald N, Kouvelas D, Prast H, Hoeger H, Lubec B (1999b) Histological changes and neurotransmitter levels three months following perinatal asphyxia in the rat. Life Sci 64:2109–2124CrossRef

Loidl CF, Herrera-Marschitz M, Anderson K, You Z-B, Goiny M, O’Connor WT, Silveira R, Rawal R, Bjelke B, Chen Y, Ungerstedt U (1994) Long-term effects of perinatal asphyxia on basal ganglia neurotransmitter systems studied with microdialysis in rat. Neurosci Lett 175:9–12PubMedCrossRef

Low JA (2004) Determining the contribution of asphyxia to brain damage in the neonate. J Obstet Gynaecol Res 30:276–286PubMedCrossRef

Lupton BA, Hill A, Roland EH, Withfield M, Flodmark O (1988) Brain swelling in the asphyxiated term newborn: pathogenesis and outcome. Pediatrics 82:139–146PubMed

Miller SP, Ramaswamy V, Michelson D, Barkovich J, Holshouser B, Wycliff N, Glidden DV, Deming D, Partridge JC, Wu YW, Ashwal S, Ferreiro DM (2005) Patterns of brain injury in term neonatal encephalopathy. J Pediatr 146:453–460PubMedCrossRef

Morales P, Klawitter V, Johansson S, Huaiquin P, Barros VG, Avalos AM, Fiedler J, Bustamante D, Gomez-Urquijo S, Goiny M, Herrera-Marschitz M (2003) Perinatal asphyxia impairs connectivity and dopamine neurite branching in organotypic triple culture from rat substantia nigra. Neurosci Lett 348:175–179PubMedCrossRef

Nakajima H, Kakui N, Ohkuma K, Ishikawa M, Hasegawa T (2005) A newly synthesized Poly(ADP-Ribose) Polymerase inhibitor, DR2313[2-methyl-3,5,7,8-tetrahydrothiopyranol[4,3-d]-pyrimidine-4-one]: pharmacological profiles, neuroprotective effects and therapeutic time window in cerebral ischemia in rats. J Pharmacol Exp Ther 312:472–481PubMedCrossRef

Pasternak JF, Predey TA, Mikhael MA (1991) Neonatal asphyxia: vulnerability of basal ganglia, thalamus and brain stem. Pediatr Neurol 7:147–149PubMedCrossRef

Pastuzko A (1994) Metabolic responses of the dopaminergic system during hypoxia in newborn brain. Biochem Med Metab Biol 51:1–15CrossRef

Paxinos G, Watson C (1982) The rat brain in stereotaxic coordinates. Academic Press, New York

Pusinelli WA, Brierley JB, Plum F (1982) Temporal profile of neuronal damage in a model of transient forebrain ischemia. Ann Neurol 11:491–498CrossRef

Roland EH, Poskitt K, Rodriguez E, Lupton BA, Hill A (1998) Perinatal hypoxic-ischemia thalamic injury: clinical features and neuroimaging. Ann Neurol 44:161–166PubMedCrossRef

Sakakibara Y, Mitha AP, Ogilvy CS, Maynard KI (2000) Post-treatment with nicotinamide (vitamin B(3)) reduces the infarct volume following permanent focal cerebral ischemia in female Sprague-Dawley and Wistar rats. Neurosci Lett 281:111–114PubMedCrossRef

Takahashi K, Pieper AA, Croul SE, Zhang J, Snyder SH, Greenberg JH (1999) Post-treatment with an inhibitor of poly(ADP-ribose) polymerase attenuates cerebral damage in focal ischemia. Brain Res 829:46–54PubMedCrossRef

Ungerstedt U (1971) Stereotaxic mapping of the monoamine pathway in the rat brain. Acta Physiol Scand Suppl 367:1–48PubMed

Ungerstedt U, Herrera-Masrschitz M, Jungnelius U, Ståhle L, Tossman U, Zetterström (1982) Dopamine synaptic mechanisms reflected in studies combining behavioural recordings and brain dialysis. Adv Biosci 37:219–231

Ungethüm U, Chen Y, Gross J, Bjelke B, Bolme P, Eneroth P, Heldt J, Loidl CF, Herrera-Marschitz M, Andersson K (1996) Effects of perinatal asphyxia on the mesostriatal/mesolimbic dopamine system of neonatal and 4-week-old male rats. Exp Brain Res 112:403–410PubMedCrossRef

Vannuci SJ, Hagberg H (2004) Hypoxia-ischemia in the immature brain. J Exp Biol 207:3149–3154CrossRef

Venkatesan A, Frucht S (2006) Movement disorders after resuscitation from cardiac arrest. Neurol Clin 24:123–132PubMedCrossRef

Virag L, Szabo C (2002) The therapeutic potential of poly(ADP-ribose) polymerase inhibitors. Pharmacol Rev 54:375–429PubMedCrossRef

Volpe J (2001) Neurology of the newborn, 4th edn. WB Saunders Company, Philadelphia, PA

Wan FJ, Lin HC, Kang BH, Tseng CJ, Tung CS (1999) D-amphetamine-induced depletion of energy and dopamine in the rat striatum is attenuated by nicotinamide pretreatment. Brain Res Bull 50:167–171PubMedCrossRef

Yan Q, Briehl M, Crowley CL, Payne CM, Bernstein H, Bernstein C (1999) The NAD+ precursors, nicotinic acid and nicotinamide upregulate glyceraldehyde-3-phosphate dehydrogenase and glucose-6-phosphate dehydrogenase mRNA in Jurkat cells. Biochem Biophys Res Commun 255:133–136PubMedCrossRef

Ying W, Alano CC, Garnier P, Swanson RA (2005) NAD+ as a metabolic link between DNA damage and cell death. J Neurosci Res 79:216–223PubMedCrossRef

Yu SW, Poitras MF, Coombs C, Bowers WJ, Federoff HJ, Poirier GC, Dawson TM, Dawson VL (2002) Mediation of poly(ADP-ribose) polymerase-1 dependent cell death by apoptosis-inducing factor. Science 297:250–263CrossRef

Zetterström T, Sharp T, Marsden C, Ungerstedt U (1983) In vivo measurement of dopamine and its metabolites by intracerebral dialysis: changes after D-amphetamine. J Neurochem 41:1769–1773PubMedCrossRef

Zhang J, Pieper A, Snyder SH (1995) Poly(ADP-ribose) synthase activation: an early indicator of neurotoxic DNA damage. J Neurochem 65:1411–1414PubMedCrossRef

Titel: Nicotinamide prevents the effect of perinatal asphyxia on dopamine release evaluated with in vivo microdialysis 3 months after birth
verfasst von: Diego Bustamante
Paola Morales
Jorge Torres Pereyra
Michel Goiny
Mario Herrera-Marschitz
Publikationsdatum: 01.03.2007
Verlag: Springer-Verlag
Erschienen in: Experimental Brain Research / Ausgabe 3/2007
Print ISSN: 0014-4819
Elektronische ISSN: 1432-1106
DOI: https://doi.org/10.1007/s00221-006-0679-0

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