Long-term effects of neonatal ischemic-hypoxic brain injury on sensorimotor and locomotor tasks in rats

Jansen, Elizabeth M.; Low, Walter C.

doi:10.1016/0166-4328(95)00248-0

Cited by 91 publications

(51 citation statements)

References 31 publications

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“…Using a battery of tests, Bona et al (30) found impairments in sensorimotor ability at 5-6 wk after HI. Similar findings were reported by Jansen et al (31) in somewhat older (up to 9 wk) animals. In contrast, results of Ikeda et al (32) demonstrated only subtle sensorimotor deficits 4 -18 wk after neonatal HI.…”

Section: Effects Of Hypoxic Preconditioningsupporting

confidence: 80%

Hypoxic Preconditioning Confers Long-Term Reduction of Brain Injury and Improvement of Neurological Ability in Immature Rats

et al. 2005

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Exposure to preconditioning (PC) hypoxia 24 h before a severe hypoxic-ischemic (HI) insult reduces development of injury in the immature brain. Several protective regimens have proved effective in the short-term but not in the long-term perspective. The aim of the present study, therefore, was to evaluate the PC effect on long-term morphologic and neurologic outcome in the developing brain. Six-day-old rats were subjected to hypoxia (36°C, 8.0% O 2 ; PC/HI group) and sham controls to normoxia (36°C; HI group) for 3 h. Twenty-four hours later, all rats were exposed to cerebral HI produced by unilateral carotid artery occlusion combined with 1 h, 15 min of hypoxia (36°C, 7.7% O 2 ). A cylinder test was used to evaluate forelimb asymmetry to determine sensorimotor function at 4, 6, and 8 wk of age. Spatial/cognitive ability was assessed by Morris water maze trials at 7 wk of recovery. Neuropathologic analysis was performed 8 wk after insult. Brain damage was reduced (p Ͻ Hypoxic-ischemic (HI) brain injury during the perinatal period is a major cause of lifelong disability (1,2). The development of effective therapeutic and/or preventive strategies to treat these pathologic events relies on a better understanding of the critical pathophysiologic events that lead to HI brain injury.In 1986, Murry et al. (3) reported that the extent of myocardial infarction resulting from a sustained coronary occlusion was diminished when the heart had been subjected to brief periods of sublethal ischemia. The protection elicited by a previous sublethal intervention that renders the tissue less sensitive to a subsequent insult has been termed preconditioning (PC). PC can be induced in the CNS through a variety of exposures, for example, seizures (4), hypoxia (5), lipopolysaccharide (6), and mitochondrial toxins (7).A PC model has been developed for the immature brain, whereby exposure to 8% hypoxia 24 h before severe HI reduces injury by 70 -100% (5,8,9). Findings of protection have been demonstrated from 1 to 3 wk after insult. Recent studies indicate, however, that development of injury in the immature brain after HI may be delayed for up to 8 wk (10), and in some cases, the salutary effects of PC in the adult (11) are partly lost after long recovery periods after the severe insult. A number of treatments after HI in immature animals have also been shown to delay injury rather than provide a permanent protection (12). Furthermore, deficits in spatial/ cognitive and sensorimotor functions sometimes occur despite no or subtle brain injury, implicating the need for sophisticated functional assessments as a complement to evaluation of lesion size (13). Our aim, therefore, was to further characterize PC in the immature brain and to determine to what extent hypoxic PC provides long-lasting behavioral and histologic protection.

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Section: Effects Of Hypoxic Preconditioningsupporting

confidence: 80%

Hypoxic Preconditioning Confers Long-Term Reduction of Brain Injury and Improvement of Neurological Ability in Immature Rats

et al. 2005

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“…4,27 In contrast, Jansen et al reported significant impairment of sensorimotor neurofunction in rats assessed by the rota-rod test at 6 to 9 weeks after HI. 5 These conflicting data reported by different authors who using the same model might be explained by differing degrees of brain injury in the cohort of HI-affected rats. A very well-designed study 4 of neuropathological and functional outcomes of neonatal HIE in adult rats revealed that only 11 of 23 (47%) of animals developed severe brain damage with significant tissue loss and porencephaly.…”

Section: Discussionmentioning

confidence: 49%

“…[1][2][3] Given the great plasticity of the developing brain, functional measures of injury are likely to be more clinically relevant. Although neurofunctional deficit after an HI insult in rats has been reported, 4,5 in mice neurofunctional studies have been applied in an adult mouse stroke model and were limited to assessment of short-term (24 hours to 4 days after stroke) neurobehavioral recovery. 6,7 There is only a single report 8 describing short-term neuroanatomical and neurofunctional outcomes of HIE in mice.…”

mentioning

confidence: 99%

Late Measures of Brain Injury After Neonatal Hypoxia–Ischemia in Mice

Ten

Tang

et al. 2004

Stroke

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Background and Purpose-This work was undertaken to determine to what degree long-term neurofunctional outcome of neonatal hypoxic-ischemic (HI) brain injury in mice correlates with anatomical extent of cerebral damage assessed by magnetic resonance imaging (MRI) and histopathology. Methods-On postnatal day 7, mice were subjected to HI. At 7 to 9 weeks after HI neurofunctional outcome was assessed by water-maze, rota-rod, and open-field test performance, followed by cerebral MRI and histopathology evaluation.

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“…25,26 The present study is the first to demonstrate clear functional effects of ischemic brain injury at P7 that remain into adult life.…”

Section: Behavioral Evaluationmentioning

confidence: 99%

Aggravated Brain Damage After Hypoxic Ischemia in Immature Adenosine A _2A Knockout Mice

Ådén

Halldner²,

Lagercrantz³

et al. 2003

Stroke

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Long-term effects of neonatal ischemic-hypoxic brain injury on sensorimotor and locomotor tasks in rats

Cited by 91 publications

References 31 publications

Hypoxic Preconditioning Confers Long-Term Reduction of Brain Injury and Improvement of Neurological Ability in Immature Rats

Hypoxic Preconditioning Confers Long-Term Reduction of Brain Injury and Improvement of Neurological Ability in Immature Rats

Late Measures of Brain Injury After Neonatal Hypoxia–Ischemia in Mice

Aggravated Brain Damage After Hypoxic Ischemia in Immature Adenosine A _2A Knockout Mice

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Long-term effects of neonatal ischemic-hypoxic brain injury on sensorimotor and locomotor tasks in rats

Cited by 91 publications

References 31 publications

Hypoxic Preconditioning Confers Long-Term Reduction of Brain Injury and Improvement of Neurological Ability in Immature Rats

Hypoxic Preconditioning Confers Long-Term Reduction of Brain Injury and Improvement of Neurological Ability in Immature Rats

Late Measures of Brain Injury After Neonatal Hypoxia–Ischemia in Mice

Aggravated Brain Damage After Hypoxic Ischemia in Immature Adenosine A 2A Knockout Mice

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Aggravated Brain Damage After Hypoxic Ischemia in Immature Adenosine A _2A Knockout Mice