Perinatal asphyxia induces region-specific long-term changes in mRNA levels of tyrosine hydroxylase and dopamine D1 and D2 receptors in rat brain

Gross, Johann; Müller, I.; Chen, Yong; Elizalde, Montserrat; Leclere, Norbert; Herrera‐Marschitz, Mario; Andersson, Kurt

doi:10.1016/s0169-328x(00)00106-6

Cited by 42 publications

(13 citation statements)

References 35 publications

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“…Our previous study confirmed that vulnerability, assayed with immunochemistry (Andersson et al 1995; Dell’Anna et al 1997; Chen et al 1997a, b; Morales et al 2003, 2005; Klawitter et al 2005), molecular biology (Andersson et al 1995; Gross et al 2000, 2005), in vivo (Dell’Anna et al 1995;1997; Chen et al 1997c), in vitro (Morales et al 2003; Klawitter et al 2005, 2006, 2007) and/or ex vivo (Ungethüm et al 1996; Chen et al 1997c; Bustamante et al 2003) biochemistry, supporting the idea that the regional impact of the insult is related to (i) the severity (extent) of the insult; (ii) the metabolic imbalance during the re-oxygenation period, and (iii) the developmental stage of the affected region.…”

Section: Regional and Developmental Vulnerabilitysupporting

confidence: 74%

Perinatal asphyxia: current status and approaches towards neuroprotective strategies, with focus on sentinel proteins

et al. 2010

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Delivery is a stressful and risky event menacing the newborn. The mother-dependent respiration has to be replaced by autonomous pulmonary breathing immediately after delivery. If delayed, it may lead to deficient oxygen supply compromising survival and development of the central nervous system. Lack of oxygen availability gives rise to depletion of NAD+ tissue stores, decrease of ATP formation, weakening of the electron transport pump and anaerobic metabolism and acidosis, leading necessarily to death if oxygenation is not promptly re-established. Re-oxygenation triggers a cascade of compensatory biochemical events to restore function, which may be accompanied by improper homeostasis and oxidative stress. Consequences may be incomplete recovery, or excess reactions that worsen the biological outcome by disturbed metabolism and/or imbalance produced by over-expression of alternative metabolic pathways. Perinatal asphyxia has been associated with severe neurological and psychiatric sequelae with delayed clinical onset. No specific treatments have yet been established. In the clinical setting, after resuscitation of an infant with birth asphyxia, the emphasis is on supportive therapy. Several interventions have been proposed to attenuate secondary neuronal injuries elicited by asphyxia, including hypothermia. Although promising, the clinical efficacy of hypothermia has not been fully demonstrated. It is evident that new approaches are warranted. The purpose of this review is to discuss the concept of sentinel proteins as targets for neuroprotection. Several sentinel proteins have been described to protect the integrity of the genome (e.g. PARP-1; XRCC1; DNA ligase IIIα; DNA polymerase β, ERCC2, DNA-dependent protein kinases). They act by eliciting metabolic cascades leading to (i) activation of cell survival and neurotrophic pathways; (ii) early and delayed programmed cell death, and (iii) promotion of cell proliferation, differentiation, neuritogenesis and synaptogenesis. It is proposed that sentinel proteins can be used as markers for characterising long-term effects of perinatal asphyxia, and as targets for novel therapeutic development and innovative strategies for neonatal care.

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Section: Regional and Developmental Vulnerabilitysupporting

confidence: 74%

Perinatal asphyxia: current status and approaches towards neuroprotective strategies, with focus on sentinel proteins

et al. 2010

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“…Tyrosine hydroxylase mRNA levels were increased in VTA and substantia nigra of perinatally asphyxiated rats suggesting increased dopamine synthesis consistent with increased turnover. Dopamine D1 receptor (DRD1) and D2 receptor (DRD2) mRNA levels were increased in the striatum suggesting altered release of dopamine (Gross et al, 2000). These findings demonstrate the complex temporal sequence of compensatory changes that occur in monoaminergic systems following perinatal insult to the nervous system and implicate all three monoaminergic systems in spatial memory impairment.…”

Section: Anoxia In Neonatal Ratmentioning

confidence: 70%

Neurobiology of animal models of attention-deficit hyperactivity disorder

Russell

2007

Journal of Neuroscience Methods

132

108

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“…Tyrosine hydroxylase mRNA levels were increased in VTA and substantia nigra of perinatally asphyxiated rats suggesting increased dopamine synthesis consistent with increased turnover. However, DRD1 and DRD2 mRNA levels were increased in the striatum suggesting impaired release of dopamine [185]. These findings demonstrate the complex temporal sequence of compensatory changes that occur in monoaminergic systems following perinatal insult to the nervous system and implicate all three monoaminergic systems in spatial memory impairment.…”

Section: Introductionmentioning

confidence: 94%

Animal models of attention-deficit hyperactivity disorder

2005

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Although animals cannot be used to study complex human behaviour such as language, they do have similar basic functions. In fact, human disorders that have animal models are better understood than disorders that do not. ADHD is a heterogeneous disorder. The relatively simple nervous systems of rodent models have enabled identification of neurobiological changes that underlie certain aspects of ADHD behaviour. Several animal models of ADHD suggest that the dopaminergic system is functionally impaired. Some animal models have decreased extracellular dopamine concentrations and upregulated postsynaptic dopamine D1 receptors (DRD1) while others have increased extracellular dopamine concentrations. In the latter case, dopamine pathways are suggested to be hyperactive. However, stimulus-evoked release of dopamine is often decreased in these models, which is consistent with impaired dopamine transmission. It is possible that the behavioural characteristics of ADHD result from impaired dopamine modulation of neurotransmission in cortico-striato-thalamo-cortical circuits. There is considerable evidence to suggest that the noradrenergic system is poorly controlled by hypofunctional α2-autoreceptors in some models, giving rise to inappropriately increased release of norepinephrine. Aspects of ADHD behaviour may result from an imbalance between increased noradrenergic and decreased dopaminergic regulation of neural circuits that involve the prefrontal cortex. Animal models of ADHD also suggest that neural circuits may be altered in the brains of children with ADHD. It is therefore of particular importance to study animal models of the disorder and not normal animals. Evidence obtained from animal models suggests that psychostimulants may not be acting on the dopamine transporter to produce the expected increase in extracellular dopamine concentration in ADHD. There is evidence to suggest that psychostimulants may decrease motor activity by increasing serotonin levels. In addition to providing unique insights into the neurobiology of ADHD, animal models are also being used to test new drugs that can be used to alleviate the symptoms of ADHD.

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Perinatal asphyxia induces region-specific long-term changes in mRNA levels of tyrosine hydroxylase and dopamine D1 and D2 receptors in rat brain

Cited by 42 publications

References 35 publications

Perinatal asphyxia: current status and approaches towards neuroprotective strategies, with focus on sentinel proteins

Perinatal asphyxia: current status and approaches towards neuroprotective strategies, with focus on sentinel proteins

Neurobiology of animal models of attention-deficit hyperactivity disorder

Animal models of attention-deficit hyperactivity disorder

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