25 years of research on global asphyxia in the immature rat brain

Barkhuizen, Melinda; Hove, Daniël L.A. van den; Vles, Johan S.H.; Steinbusch, Harry W.; Kramer, Boris W.; Gavilanes, Antonio W. D.

doi:10.1016/j.neubiorev.2017.01.042

Cited by 40 publications

(53 citation statements)

References 152 publications

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“…Animal models of oxygen deprivation in neonates have been developed for studying this clinical condition. Neonatal hypoxia‐ischemia (Vannucci and Vannucci, 2005; Levine, 1960), perinatal asphyxia (Barkhuizen et al, 2017) and neonatal anoxia (Takada et al, 2011) in rats are included in the most often used models in newborns. Neonatal anoxia in rats causes loss in neuronal and glial populations in brain areas, cognitive and behavioral deficits (Takada et al, 2016, 2015; Kumar et al, 2017, 2019), delay in sensorimotor development and changes in somatic growth (Kumar et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Neonatal anoxia impairs long‐term energy metabolism and somatic development of Wistar rats

Cruz-Ochoa

Ochoa-Amaya

Pulecio

et al. 2019

Intl J of Devlp Neuroscience

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Background: Neonatal anoxia may cause neurological injuries, behavioral alterations and changes in somatic growth. Somatic developmental changes suggest a possible effect of anoxia on energy metabolism and/or feeding behavior. Short-term effects of oxygen deficit on energy homeostasis have been described. In contrast, just a few studies report long-term effects. This study investigated the effects of neonatal anoxia on energy metabolism and somatic development at adulthood of males and females Wistar rats. Method: Male (m) and female (f) rats were exposed, on postnatal day 2 (P2), to either 25-min of Anoxia or Control treatment. At P34 part of the subjects of each group was fasted for 18 h, refeed for 1 h and then perfused 30 min later, at P35; the remaining subjects were submitted to these treatments at P94 and perfused at P95. Therefore, there were 8 groups: AmP35, AmP95, AfP35, AfP95, CmP35, CmP95, CfP35 and CfP95. For subjects perfused at P95, body weight and food intake were recorded up to P90. For subjects perfused at P35 and P95, glycemia, leptin and insulin were assessed after fasting and refeed. After perfusion the encephalon and pancreas were collected for Fos immunohistochemistry and Hematoxylin-Eosin stain analyses. Results: Even though neonatal anoxia did not interfere with regular food intake, it reduced body weight gain along growing in both male and female subjects as compared to the corresponding controls. At P35 neonatal anoxia decreased post-prandial glycemia and increased insulin. While at P95 neonatal anoxia altered the pancreatic histomorphology and increased post-fasting weight loss, decreasing leptin, insulin and glycemia secretion, as well Fos immunoreactivity (IR) in ARC. Conclusion: Neonatal anoxia impairs long-term energy metabolism and somatic development in Wistar rats, with differences related to sex and age.

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Section: Introductionmentioning

confidence: 99%

Neonatal anoxia impairs long‐term energy metabolism and somatic development of Wistar rats

Cruz-Ochoa

Ochoa-Amaya

Pulecio

et al. 2019

Intl J of Devlp Neuroscience

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“…From our point of view, the PND7 model is not the better option to study this specific damage in GABAergic neurons. In fact, this effect of PA has been mostly reported using the PND0 models (Barkhuizen et al, 2017). Each zone and the biochemical event should be analyzed in particular.…”

Section: Limitationsmentioning

confidence: 96%

Deep hypothermia reverses behavioral and histological alterations in a rat model of perinatal asphyxia

Vazquez

Peña

Rojo

et al. 2018

J of Comparative Neurology

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The consequences of perinatal asphyxia (PA) include alterations which may manifest as schizophrenia. Characteristic features of this disease include a decrease in specific subpopulations of GABAergic cells and deterioration of social interaction. The purpose of this study is to assess if a deep and short‐hypothermic treatment can ameliorate this damage in a model of PA. Rats offsprings were exposed to 19 min of asphyxia by immersing the uterus horns in water at 37 °C followed by 30 min in air at 10 °C that resulted in 15 °C body temperature. At postnatal day 36–38, the rats were tested in the open field and social interaction paradigms and processed for immunostaining of calbindin and reelin. A brief exposure to deep hypothermia reversed the deterioration produced by PA in play soliciting. PA decreased the density of calbindin neurons in layer II of the Anterior Insular Cortex, while deep hypothermia reversed this effect. Paradoxically, in AIC, there was a significant increase in the number of reelin‐secreting neurons in layers II and III generated by PA and this increase was reversed by hypothermia. This suggests a compensatory mechanism, where reelin neurons trend to compensate for the loss of calbindin neurons, at least within Anterior Insular Cortex. Finally, the deep hypothermic shock might represent a valuable therapeutic alternative to treat PA.

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“…Fifty-three male rat pups were subjected to PA using an experimental model (Bjelke et al, 1991), which produces moderate to severe PA (Van de Berg et al, 2003;Galeano et al, 2011) as we described previously (Capani et al, 2003(Capani et al, , 2009Saraceno et al, 2010Saraceno et al, , 2012aBlanco et al, 2015;Holubiec et al, 2017;Herrera et al, 2018). The murine model of PA, originally developed by Bjelke et al (1991), has been widely used (Barkhuizen et al, 2017;Herrera et al, 2017b) and accepted to mimic this condition (Capani et al, 1997(Capani et al, , 2003(Capani et al, , 2009Boksa and El-Khodor, 2003;Saraceno et al, 2010Saraceno et al, , 2012aStrackx et al, 2010;Muñiz et al, 2014;Romero et al, 2015;Wakuda et al, 2015;Herrera et al, 2018). The Bjelke model presents several advantages such as follows: (a) asphyxia is produced at birth (Capani et al, 2009); (b) acidosis, hypercapnia, and hypoxia are present in the whole body, replicating a global asphyxia, which is the most common type (Strackx et al, 2010); (c) it is non-invasive, avoiding the effects of surgical procedures; and (d) since hypoxia is produced in the whole body, it affects both brain hemispheres, which makes this model more suitable for behavioral studies (Arteni et al, 2010).…”

Section: Induction Of Pamentioning

confidence: 99%

Partial Reversal of Striatal Damage by Palmitoylethanolamide Administration Following Perinatal Asphyxia

et al. 2020

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Perinatal asphyxia (PA) is a clinical condition brought by a birth temporary oxygen deprivation associated with long-term damage in the corpus striatum, one of the most compromised brain areas. Palmitoylethanolamide (PEA) is a neuromodulator well known for its protective effects in brain injury models, including PA, albeit not deeply studied regarding its particular effects in the corpus striatum following PA. Using Bjelke et al. (1991) PA model, full-term pregnant rats were decapitated, and uterus horns were placed in a water bath at 37 • C for 19 min. One hour later, the pups were injected with PEA 10 mg/kg s.c., and placed with surrogate mothers. After 30 days, the animals were perfused, and coronal striatal sections were collected to analyze protein-level expression by Western blot and the reactive area by immunohistochemistry for neuron markers: phosphorylated neurofilament-heavy/medium-chain (pNF-H/M) and microtubule-associated protein-2 (MAP-2), and the astrocyte marker, glial fibrillary acidic protein (GFAP). Results indicated that PA produced neuronal damage and morphological changes. Asphyctic rats showed a decrease in pNF-H/M and MAP-2 reactive areas, GFAP + cells number, and MAP-2 as well as pNF-H/M protein expression in the striatum. Treatment with PEA largely restored the number of GFAP + cells. Most important, it ameliorated the decrease in pNF-H/M and MAP-2 reactive areas in asphyctic rats. Noticeably, PEA treatment reversed the decrease in MAP-2 protein expression and largely prevented PA-induced decrease in pNF-H/M protein expression. PA did not affect the GFAP protein level. Treatment with PEA attenuated striatal damage induced by PA, suggesting its therapeutic potential for the prevention of neurodevelopmental disorders.

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25 years of research on global asphyxia in the immature rat brain

Cited by 40 publications

References 152 publications

Neonatal anoxia impairs long‐term energy metabolism and somatic development of Wistar rats

Neonatal anoxia impairs long‐term energy metabolism and somatic development of Wistar rats

Deep hypothermia reverses behavioral and histological alterations in a rat model of perinatal asphyxia

Partial Reversal of Striatal Damage by Palmitoylethanolamide Administration Following Perinatal Asphyxia

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