scholarly journals Delayed injury of hippocampal interneurons after neonatal hypoxia-ischemia and therapeutic hypothermia in a murine model

Hippocampus ◽  
2018 ◽  
Vol 28 (8) ◽  
pp. 617-630 ◽  
Author(s):  
Raul Chavez-Valdez ◽  
Paul Emerson ◽  
Janasha Goffigan-Holmes ◽  
Alfredo Kirkwood ◽  
Lee J. Martin ◽  
...  
Keyword(s):  
Therapeutic Hypothermia ◽  
Murine Model ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

scholarly journals Calbindin-1 Expression in the Hippocampus following Neonatal Hypoxia-Ischemia and Therapeutic Hypothermia and Deficits in Spatial Memory

2018 ◽  
Vol 40 (5-6) ◽  
pp. 508-522 ◽  
Author(s):  
Janasha Goffigan-Holmes ◽  
Dafne Sanabria ◽  
Johana Diaz ◽  
Debra Flock ◽  
Raul Chavez-Valdez
Keyword(s):  
Therapeutic Hypothermia ◽  
Neurodegenerative Disorders ◽  
Memory Impairment ◽  
Memory Deficits ◽  
Nissl Staining ◽  
Memory Impairments ◽  
Neonatal Hypoxia ◽  
Y Maze ◽  
Hypoxia Ischemia ◽  
With Memory

Hippocampal injury following neonatal hypoxia-ischemia (HI) leads to memory impairments despite therapeutic hypothermia (TH). In the hippocampus, the expression of calbindin-1 (Calb1), a Ca2+-buffering protein, increases during postnatal development and decreases with aging and neurodegenerative disorders. Since persistent Ca2+ dysregulation after HI may lead to ongoing injury, persistent changes in hippocampal expression of Calb1 may contribute to memory impairments after neonatal HI. We hypothesized that, despite TH, neonatal HI persistently decreases Calb1 expression in the hippocampus, a change associated with memory deficits in the mouse. We induced cerebral HI in C57BL6 mice at postnatal day 10 (P10) with right carotid ligation and 45 min of hypoxia (FiO2 = 0.08), followed by normothermia (36°C, NT) or TH (31°C) for 4 h with anesthesia-shams as controls. Nissl staining and glial fibrillary acidic protein (GFAP) immunohistochemistry (IHC) were used to grade brain injury and astrogliosis at P11, P18, and P40 prior to the assessment of Calb1 expression by IHC. The subset of mice followed to P40 also performed a memory behavior task (Y-maze) at P22–P26. Nonparametric statistics stratified by sex were applied. In both anterior and posterior coronal brain sections, hippocampal Calb1 expression doubled between P11 and P40 due to an increase in the cornus ammonis (CA) field (Kruskal-Wallis [KW] p < 0.001) and not the dentate gyrus (DG). Neonatal HI produced delayed (P18) and late (P40) deficits in the expression of Calb1 exclusively in the CA field (KW p = 0.02) in posterior brain sections. TH did not attenuate Calb1 deficits after HI. Thirty days after HI injury (at P40), GFAP scores in the hippocampus (p < 0.001, r = –0.47) and CA field (p < 0.001, r = –0.39) of posterior brain sections inversely correlated with their respective Calb1 expression. Both sexes demonstrated deficits in Y-maze testing, including approximately 40% lower spontaneous alterations performance and twice as much total impairment compared to sham mice (KW p < 0.001), but it was only in females that these deficits correlated with the Calb1 expression in the hippocampal CA field (p < 0.05) of the posterior sections. Hippocampal atrophy after neonatal HI also correlated with worse deficits in Y-maze testing, but it did not predict Calb1 deficits. Neonatal HI produces a long-lasting Calb1 deficit in the hippocampal CA field during development, which is not mitigated by TH. Late Calb1 deficit after HI may be the result of persistent astrogliosis and can lead to memory impairment, particularly in female mice.

scholarly journals Effects of therapeutic hypothermia on white matter injury from murine neonatal hypoxia–ischemia

2017 ◽  
Vol 82 (3) ◽  
pp. 518-526 ◽  
Author(s):  
Elliot Koo ◽  
R Ann Sheldon ◽  
Byong Sop Lee ◽  
Zinaida S Vexler ◽  
Donna M Ferriero
Keyword(s):  
White Matter ◽  
Therapeutic Hypothermia ◽  
White Matter Injury ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

scholarly journals Therapeutic hypothermia achieves neuroprotection via a decrease in acetylcholine with a concurrent increase in carnitine in the neonatal hypoxia‐ischemia (877.2)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Mayumi Kajimura ◽  
Toshiki Takenouchi ◽  
Tsuyoshi Nakanishi ◽  
Yuki Sugiura ◽  
Takako Hishiki ◽  
...  
Keyword(s):  
Therapeutic Hypothermia ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

scholarly journals Activation of autophagy and Akt/CREB signaling play an equivalent role in the neuroprotective effect of rapamycin in neonatal hypoxia-ischemia

Autophagy ◽  
2010 ◽  
Vol 6 (3) ◽  
pp. 366-377 ◽  
Author(s):  
Silvia Carloni ◽  
Silvia Girelli ◽  
Claudia Scopa ◽  
Giuseppe Buonocore ◽  
Mariangela Longini ◽  
...  
Keyword(s):  
Neuroprotective Effect ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

scholarly journals The nonerythropoietic asialoerythropoietin protects against neonatal hypoxia-ischemia as potently as erythropoietin

2004 ◽  
Vol 91 (4) ◽  
pp. 900-910 ◽  
Author(s):  
Xiaoyang Wang ◽  
Changlian Zhu ◽  
Xinhua Wang ◽  
Jens Gammeltoft Gerwien ◽  
Andre Schrattenholz ◽  
...  
Keyword(s):  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

scholarly journals Splenic Immune Cells in Experimental Neonatal Hypoxia–Ischemia

2012 ◽  
Vol 4 (2) ◽  
pp. 208-219 ◽  
Author(s):  
Nancy Fathali ◽  
Robert P. Ostrowski ◽  
Yu Hasegawa ◽  
Tim Lekic ◽  
Jiping Tang ◽  
...  
Keyword(s):  
Immune Cells ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

Neonatal hypoxia-ischemia caused mild motor dysfunction, recovered by acrobatic training, without affecting morphological structures involved in motor control in rats

2019 ◽  
Vol 1707 ◽  
pp. 27-44 ◽  
Author(s):  
Heloísa Deola Confortim ◽  
Bruna Ferrary Deniz ◽  
Wellington de Almeida ◽  
Patrícia Maidana Miguel ◽  
Loise Bronauth ◽  
...  
Keyword(s):  
Motor Control ◽  
Motor Dysfunction ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

Experimental neonatal hypoxia ischemia causes long lasting changes of oxidative stress parameters in the hippocampus and the spleen

2018 ◽  
Vol 46 (4) ◽  
pp. 433-439 ◽  
Author(s):  
Felipe Kawa Odorcyk ◽  
Janaína Kolling ◽  
Eduardo Farias Sanches ◽  
Angela T.S. Wyse ◽  
Carlos Alexandre Netto
Keyword(s):  
Oxidative Stress ◽  
Wistar Rat ◽  
Mortality And Morbidity ◽  
Neonatal Hypoxia ◽  
Oxidative Stress Parameters ◽  
Rat Pups ◽  
Hypoxia Ischemia ◽  
Anti Oxidant ◽  
Enzyme Superoxide Dismutase ◽  
Stress Parameters

Abstract Neonatal hypoxia ischemia (HI) is the main cause of mortality and morbidity in newborns. The mechanisms involved in its progression start immediately and persist for several days. Oxidative stress and inflammation are determinant factors of the severity of the final lesion. The spleen plays a major part in the inflammatory response to HI. This study assessed the temporal progression of HI-induced alterations in oxidative stress parameters in the hippocampus, the most affected brain structure, and in the spleen. HI was induced in Wistar rat pups in post-natal day 7. Production of reactive oxygen species (ROS), and the activity of the anti oxidant enzyme superoxide dismutase and catalase were assessed 24 h, 96 h and 38 days post-HI. Interestingly, both structures showed a similar pattern, with few alterations in the production of ROS species up to 96 h often combined with an increased activity of the anti oxidant enzymes. However, 38 days after the injury, ROS were at the highest in both structures, coupled with a decrease in the activity of the enzymes. Altogether, present results suggest that HI causes long lasting alterations in the hippocampus as well as in the spleen, suggesting a possible target for delayed treatments for HI.

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