Episodic neonatal hypoxia evokes executive dysfunction and regionally specific alterations in markers of dopamine signaling

@article{Decker2003EpisodicNH,
  title={Episodic neonatal hypoxia evokes executive dysfunction and regionally specific alterations in markers of dopamine signaling},
  author={Michael J Decker and Gillian E. Hue and William Michael Caudle and Gary W. Miller and Graeme Keating and David B. Rye},
  journal={Neuroscience},
  year={2003},
  volume={117},
  pages={417-425}
}
Perinatal ischemic-anoxic and prolonged anoxic insults lead to impaired dopaminergic signaling and are hypothesized to contribute, at least in part, to the pathogenesis of disorders of minimal brain dysfunction such as attention-deficit hyperactivity disorder. We hypothesized that subtle intermittent hypoxic insults, occurring during a period of critical brain development, are also pathogenic to dopaminergic signaling, thereby contributing to behavioral and executive dysfunction. Between… 
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Effect of postnatal intermittent hypoxia on locomotor activity and neuronal development in rats tested in early adulthood
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TLDR
Melatonin has short- and long-term protective effects against hypoxia-induced neurobehavioral deficits in the neonatal mouse, associated with increasing neurogenesis and attenuation of cell death and inflammatory responses in the hippocampus.
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These studies indicate that intermittent hypoxia/hypercapnia leads to oxidative stress due to mitochondrial response within the mouse central nervous system.
Does neonatal brain ischemia induce schizophrenia-like behavior in young adult rats?
TLDR
Behavioral alterations induced by one hour of continuous bilateral common carotid artery occlusion in 12-day-old male rats suggest that perinatal hypoxic/ischemic insults may represent a risk factor for later manifestation of specific features relevant to schizophrenia in predisposed individuals.
The acute and delayed effects of perinatal hypoxic brain damage in children and in model experiments with rodents
TLDR
It has been shown that hypoxia triggers a cascade of biochemical and molecular processes, such as energy insufficiency, depolarization of membranes, an increase in the release of mediators and suppression of their reuptake, and production of free radicals, which damage neurons and induce neurodegeneration and cell death.
Pathological consequences of intermittent hypoxia in the central nervous system.
TLDR
The cumulative evidence confirms that IH indeed induces a heterotopic pattern of injury in the brain, particularly affecting cortical, subcortical, and hippocampal regions, ultimately leading to neuronal apoptosis and activation of microglia.
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