Relationship of extracellular dopamine in striatum of newborn piglets to cortical oxygen pressure

Huang, Chao; Lajevardi, Nasser S.; Tammela, Outi; Pastuszko, Anna; Delivoria‐Papadopoulos, Maria; Wilson, David F.

doi:10.1007/bf00967702

Cited by 48 publications

(31 citation statements)

References 31 publications

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“…In newborn piglets, it has been shown that O 2 deprivation responds with gradual increase of [DA] e as a result of reduced brain tissue PO 2 in a dose-dependent manner (13). The hypothesis that an increase of [DA] e during a hypoxic insult plays an important role in the pathogenesis of neuronal injury in newborn brain is supported by numerous findings from different injury models.…”

Section: Discussionmentioning

confidence: 98%

“…However, the dopaminergic system is also sensitive to O 2 deprivation in the immature brain (10 -12). Obviously, there is no "oxygen reserve" that protects dopamine (DA) release and metabolism from decrease in O 2 pressure, because in the newborn piglet brain, even a small reduction of the brain tissue PO 2 causes a significant increase in the striatal extracellular DA concentration in a dose-dependent relationship (13). We showed previously that H/H induces an increase of aromatic amino acid decarboxylase (AADC) activity, indicating an increase of mesostriatal dopaminergic activity in newborn piglets (14), which is known to be associated with pronounced neuronal injury as a result of hypoxicischemic brain (15,16).…”

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confidence: 99%

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Effect of Moderate Hypercapnic Hypoxia on Cerebral Dopaminergic Activity and Brain O2 Uptake in Intrauterine Growth–Restricted Newborn Piglets

et al. 2005

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Section: Discussionmentioning

confidence: 98%

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confidence: 99%

Effect of Moderate Hypercapnic Hypoxia on Cerebral Dopaminergic Activity and Brain O2 Uptake in Intrauterine Growth–Restricted Newborn Piglets

et al. 2005

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“…This is noteworthy because the immature cerebral dopaminergic system is sensitive to altered brain oxidative metabolism. There is no oxygen reserve to protect dopamine release and metabolism from a decrease in oxygen pressure because in newborn piglet brain, a reduction of brain tissue PO 2 causes a significant increase in striatal extracellular dopamine content in a dosedependent fashion (25). We have recently found that the synthesis rate of FDA from FDOPA is also increased under those circumstances (26).…”

Section: Discussionmentioning

confidence: 99%

Intrauterine Growth Restriction Induces Up-Regulation of Cerebral Aromatic Amino Acid Decarboxylase Activity in Newborn Piglets: [18F]Fluorodopa Positron Emission Tomographic Study

et al. 2001

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There is evidence that intrauterine growth restriction (IUGR) is associated with altered dopaminergic function in the immature brain. However, the relevant enzyme activities have not been measured in the living neonatal brain together with brain oxidative metabolism. Therefore, fluorine-18-labeled 6-fluoro-L-3,4-dihydroxyphenylalanine (FDOPA) was used together with positron emission tomography to estimate the activity of the aromatic amino acid decarboxylase in the brain of 10 newborn IUGR piglets (2 to 5 d old; body weight, 908 Ϯ 109 g) and in 10 normal-weight (3 to 5 d old; body weight, 2142 Ϯ 373 g) newborn piglets. The regional transport of FDOPA to the brain and the clearance rate of labeled metabolites from brain tissue were broadly similar in the two groups. However, the regional rate constant for back flux from the brain was markedly increased in IUGR piglets for striatum (72%) and frontal cortex (83%) (p Ͻ 0.05). Furthermore, the rate constant for conversion of FDOPA to fluorodopamine was markedly increased (between 48% in cerebellum and 91% in mesencephalon, p Ͻ 0.05) in all brain regions of IUGR piglets studied. Thus, it is suggested that IUGR induces an up-regulation of aromatic amino acid decarboxylase activity that is not related to alterations in brain oxidative metabolism. An inadequate nutritional supply due to uteroplacental insufficiency or restricted maternal protein intake late in gestation is largely responsible for asymmetrical IUGR (1). Reduced fetal growth can be viewed as a compensation for the reduced supply as long as fetal demand is not critically restricted, leading to decompensation with asphyxia and even death (2). The compromised nutritional state has adverse effects on fetal physiology and metabolism including changes of hormonal homeostasis (3), which are thought to be associated with postnatal growth failure and a greater propensity to develop cardiovascular metabolic disease or behavioral abnormalities later in life (4). Therefore, the period of fetal adaptation, characterized by reduced growth due to restricted glucose and amino acid availability but largely compensated placental respiratory function (5), reflects a functional state that may lead to both acceleration or delay in organ maturation (6, 7).The importance of the intrauterine environment for fetal brain development has been stressed by studies showing persistent behavioral abnormalities in prenatally stressed animals (8). Rats exposed to noise and light stress during the last trimester of pregnancy produce offspring with altered locomo- ABSTRACT474

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“…In the turtle, extracellular glutamate and dopamine are maintained at basal levels during extended anoxia Milton and Lutz, 1998), while levels of inhibitory neuroactive compounds such as GABA and glycine increase . By contrast, extracellular neurotransmitter levels increase indiscriminately in anoxia-intolerant animals: dopamine, aspartate, glutamate, GABA and taurine all increase in the hypoxic or anoxic neonatal rat and adult rat brain (Huang et al, 1994;PerezPinzon et al, 1993;Young et al, 1993), while glutamate, aspartate, GABA, and taurine are all released from hippocampal slices exposed to hypoxia, chemical ischemia or hydrogen peroxide (Saransaari and Oja, 1998).…”

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confidence: 99%

“…Dopamine is of particular interest because this compound is neurotoxic at high levels, but unlike other excitotoxins such as glutamate, dopamine levels increase in the mammalian extracellular compartment well before anoxic or ischemic depolarization (Huang et al, 1994;Globus et al, 1988). By contrast, extracellular dopamine levels do not increase in the anoxic turtle brain due to both decreased release (S. L. Milton and P. L. Lutz, manuscript in preparation) and continued reuptake (Milton and Lutz, 1998).…”

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Slow death in the leopard frogRana pipiens: neurotransmitters and anoxia tolerance

Milton

Manuel

Lutz

2003

Journal of Experimental Biology

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The effects of anoxia/ischemia on the mammalian brain, and the mechanisms that promote survival or neuronal failure, have been extensively studied owing to their great significance in human pathophysiology. In brief, the mammalian brain loses ATP within minutes of oxygen deprivation, with a subsequent failure of ATP-dependent ion exchangers, the loss of ionic gradients, and membrane depolarization. Depolarization then results in a cytotoxic increase in intracellular Ca 2+ concentration, the uncontrolled release of excitatory neurotransmitters to neurotoxic levels, and subsequent neuronal death (for a review, see Lutz et al., 2003). Once temperature differences are taken into account, this scenario is in fact the characteristic response of nearly all vertebrate brains, from fish to mammals (Lutz et al., 2003). A few species, however, including turtles in the genera Trachemys and Chrysemys and fish in the genus Carassius, can survive anoxia for days at 25°C and months at temperatures below 10°C (Lutz et al., 2003). These animals are able to greatly reduce brain metabolic rates to a level where energy costs are matched by anaerobic energy production; ATP levels are thus maintained and anoxic depolarization is avoided. Specific adaptations by which the brains of the anoxia-tolerant organisms survive include a reduction in membrane ion permeability (channel arrest) (Bickler et al., 2002), the release of inhibitory neurotransmitters such as GABA and alanine , and protection against the uncontrolled release of such excitotoxic compounds as glutamate and dopamine (Milton and Lutz, 1998;Milton et al., 2002).Some frog species (Rana temporaria, Rana pipiens) demonstrate an intermediate anoxia tolerance, their brains able to survive 4-5·h without oxygen at room temperature (Knickerbocker and Lutz, 2001;Lutz and Reiners, 1997) and at least 30·h without oxygen at 5°C (Hermes-Lima and Storey, 1996). This tolerance to anoxia appears to be accomplished through an overall metabolic depression, primarily via hypoperfusion of the skeletal muscle , which allows the frog to maintain ATP levels in certain organ systems. However, unlike truly anoxia-tolerant vertebrates, the frog brain does not defend ATP levels, and when energy stores reach a critical low, (approximately 35% of normoxic levels), ion homeostatic mechanisms are compromised and extracellular K + levels While frogs such as Rana temporaria are known to withstand 4-5·h anoxia at room temperature, little is known about the neurological adaptations that permit this. Previous research has shown that changes in neuroactive compounds such as glutamate and dopamine in anoxia-sensitive (mammalian) brains follow a strikingly different pattern than is observed in truly anoxia-tolerant vertebrates such as the freshwater turtle. The present study measured changes in the levels of whole brain and extracellular amino acids, and extracellular dopamine, in the normoxic and 3-4·h anoxic frog Rana pipiens, in order to determine whether their neurotransmitter responses resemble the anoxia-vu...

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Relationship of extracellular dopamine in striatum of newborn piglets to cortical oxygen pressure

Cited by 48 publications

References 31 publications

Effect of Moderate Hypercapnic Hypoxia on Cerebral Dopaminergic Activity and Brain O2 Uptake in Intrauterine Growth–Restricted Newborn Piglets

Effect of Moderate Hypercapnic Hypoxia on Cerebral Dopaminergic Activity and Brain O2 Uptake in Intrauterine Growth–Restricted Newborn Piglets

Intrauterine Growth Restriction Induces Up-Regulation of Cerebral Aromatic Amino Acid Decarboxylase Activity in Newborn Piglets: [18F]Fluorodopa Positron Emission Tomographic Study

Slow death in the leopard frogRana pipiens: neurotransmitters and anoxia tolerance

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