BDNF Protects against Spatial Memory Deficits Following Neonatal Hypoxia-Ischemia

2000 ◽  
Vol 166 (1) ◽  
pp. 99-114 ◽  
Author(s):  
C.Robert Almli ◽  
Todd J. Levy ◽  
Byung Hee Han ◽  
Aarti R. Shah ◽  
Jeffrey M. Gidday ◽  
...  
Keyword(s):  
Spatial Memory ◽  
Memory Deficits ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

Erythropoietin improves long-term spatial memory deficits and brain injury following neonatal hypoxia–ischemia in rats

2004 ◽  
Vol 153 (1) ◽  
pp. 77-86 ◽  
Author(s):  
Abdullah Kumral ◽  
Nazan Uysal ◽  
Kazim Tugyan ◽  
Atac Sonmez ◽  
Osman Yilmaz ◽  
...  
Keyword(s):  
Brain Injury ◽  
Spatial Memory ◽  
Memory Deficits ◽  
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.

Early enriched housing results in partial recovery of memory deficits in female, but not in male, rats after neonatal hypoxia–ischemia

2008 ◽  
Vol 1218 ◽  
pp. 257-266 ◽  
Author(s):  
Lenir Orlandi Pereira ◽  
Atahualpa Cauê Paim Strapasson ◽  
Patrícia Machado Nabinger ◽  
Matilde Achaval ◽  
Carlos Alexandre Netto
Keyword(s):  
Memory Deficits ◽  
Male Rats ◽  
Partial Recovery ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia ◽  
Recovery Of Memory

Effects of daily environmental enrichment on memory deficits and brain injury following neonatal hypoxia-ischemia in the rat

2007 ◽  
Vol 87 (1) ◽  
pp. 101-108 ◽  
Author(s):  
Lenir Orlandi Pereira ◽  
Nice Sarmento Arteni ◽  
Ruth Chamorro Petersen ◽  
Anderson Padilha da Rocha ◽  
Matilde Achaval ◽  
...  
Keyword(s):  
Brain Injury ◽  
Environmental Enrichment ◽  
Memory Deficits ◽  
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
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