Long-lasting behavioral alterations following a hypoxic/ischemic brain injury in neonatal rats

Balduini, Walter; Angelis, Valerio De; Mazzoni, Erika; Cimino, Mauro

doi:10.1016/s0006-8993(00)01997-1

Cited by 135 publications

(111 citation statements)

References 16 publications

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“…Only 8 out of 19 HI-subjected rats were tested in the open-field paradigm and the degree of cerebral damage in those tested animals was not specified. 27 Thus, in different species, rat and mouse, this model of HI brain injury results in various extent of cerebral damage, which ultimately predicts the degree of neurofunctional deficit as it shown in current study.…”

Section: Discussionsupporting

confidence: 66%

“…In that cohort, however, 39% of animals had mild cerebral damage without cystic lesions. 27 did not find significant differences in spontaneous and apomorphineinduced behavior in open-field between HI-subjected and control rats tested at 96 days of life. It is important to mention, as in the present study, in Balduini's experiments 11 of 19 HI-subjected rats developed severe brain injury with significant tissue loss.…”

Section: Discussioncontrasting

confidence: 61%

“…In rats subjected to HI, some authors found no long-term sensorimotor deficit assessed by the rota-rod test. 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.…”

Section: Discussionmentioning

confidence: 95%

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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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Section: Discussionsupporting

confidence: 66%

Section: Discussioncontrasting

confidence: 61%

Section: Discussionmentioning

confidence: 95%

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

Ten

Tang

et al. 2004

Stroke

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“…A few studies dealing with the longterm behavioral alterations after HI insult in neonatal rats have demonstrated obvious sensorimotor deficits, learning and memory impairment [19,28]. However, peripheral neuronal changes in adulthood associated with neonatal HI insult have not been studied enough in the experimental model of perinatal asphyxia.…”

Section: Discussionmentioning

confidence: 99%

“…Although many reports have studied the morphological and biochemical outcomes [16][17][18], and the long-lasting behavioral changes [19,20] occurring in rats after neonatal hypoxia-ischemia, little emphasis has been placed on assessing the long--lasting influence on peripheral nerves. Furthermore, there has been no study that investigates the effects of TNF-α inhibitor (etanercept) on peripheral neuronal damage in a neonatal rat model of HI.…”

mentioning

confidence: 99%

Effects of a Tumor Necrosis Factor-Alpha Inhibitor (Etanercept) on the Sciatic Nerve in a Hypoxic Ischemia-Induced Neonatal Rat Model

Büyükakıllı¹,

Atıcı²,

Ballı³

et al. 2014

Adv Clin Exp Med

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Background. Neonatal hypoxic-ischemic (HI) injury has been considered to have acute and long term deleterious effects on many tissues, including the peripheral nerve. Objectives. In this study, the effects of a tumor necrosis factor-alpha (TNF-α) inhibitor (etanercept) on peripheral nerve damage and the ultrastructure of the sciatic nerve and gastrocnemius muscle in rats exposed to HI during the neonatal period were examined. Material and Methods. In this study, 45 seven-day-old rats were used and they were divided into three groups. The right carotid arteries of the rats in the saline and etanercept groups were ligated and put in a hypoxia chamber containing 8% oxygen for two hours. Just after hypoxia, the etanercept group was given 10 mg/kg etanercept, but the saline group had only saline intraperitoneally. The sham group rats' carotid arteries were not ligated or put in hypoxia. The amplitude, area and latency of sciatic nerve compound motor action potential (CMAP), which mainly reflects axonopathy and myelinopathy, were measured using standard techniques in the seventeenth week following the HI. Sciatic nerve and gastrocnemius muscle were evaluated with a transmission electron microscope, and grading for myelin sheath damage was done to all groups. Results. Neuropathy was seen in rats after HI. While treatment with etanercept showed a protective effect for the axons of sciatic nerve, demyelination could not be recovered with etanercept. Conclusions. This study is the first in literature to show a partial interruption of the signal through the peripheral nerve fibers caused by axonal and myelin dysfunction continuation in rats exposed to HI after birth, in the 17

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Experimental Models of Hypoxic‐Ischemic Encephalopathy: Hypoxia‐Ischemia in the Immature Rat

Carloni

Balduini

2008

CP Toxicology

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The development of experimental models to study the mechanisms of perinatal hypoxic-ischemic encephalopathy and stroke and effective therapies represents an important goal in perinatal medicine. However, due to the complexity of this pathological condition in humans, to date there is no ideal animal model that completely reproduces this condition. This unit describes the most widely used rodent animal model for the study of hypoxic-ischemic encephalopathy during development. The model consists of 7-day-old pup rats subjected to unilateral carotid artery ligation followed by timed hypoxia exposure, and incorporates both focal cerebral ischemia and reperfusion. Its strength lies in the relative ease of the surgical procedure, the low mortality rate, and the possibility of performing long-term experiments, a necessity for preclinical therapeutic trials. Over the years, this model has been extensively characterized, and most information on the mechanisms responsible for neurodegeneration and possible therapeutic approaches following hypoxia-ischemia during brain development derives from studies performed using this model.

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Long-lasting behavioral alterations following a hypoxic/ischemic brain injury in neonatal rats

Cited by 135 publications

References 16 publications

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

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

Effects of a Tumor Necrosis Factor-Alpha Inhibitor (Etanercept) on the Sciatic Nerve in a Hypoxic Ischemia-Induced Neonatal Rat Model

Experimental Models of Hypoxic‐Ischemic Encephalopathy: Hypoxia‐Ischemia in the Immature Rat

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