Are the consequences of neonatal hypoxia–ischemia dependent on animals' sex and brain lateralization?

Sanches, Eduardo Farias; Arteni, Nice Sarmento; Scherer, Emilene B. S.; Kolling, Janaína; Nicola, Fabrício do Couto; Willborn, S.; Wyse, Ângela T. S.; Netto, Carlos Alexandre

doi:10.1016/j.brainres.2013.02.040

Cited by 32 publications

(26 citation statements)

References 75 publications

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“…; Sanches et al . ). We therefore used the weight ratio of the left to right cerebral hemispheres together with the neuronal density ratio of CA3 region to quantify HI‐induced brain loss/damage.…”

Section: Discussionmentioning

confidence: 97%

“…Previous studies shown that the brain weight ratio is a suitable measure of brain damage that is as sensitive as, and is in accordance with, histopathological and biochemical results (Zhao et al 2007). Neurons of cortex, basal ganglia, thalamus, and hippocampus can be affected by cerebral HI, and the hippocampal CA3 region has been reported to have a close relationship with learning and memory ability, especially the proper accomplishment in the learning and memory process (Pazos et al 2012;Sanches et al 2013). We Fig.…”

Section: Discussionmentioning

confidence: 99%

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Autophagy activation involved in hypoxic‐ischemic brain injury induces cognitive and memory impairment in neonatal rats

Tian

et al. 2016

Journal of Neurochemistry

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Hypoxic-ischemic brain injury (HIBI) in neonates can lead to lifelong cognitive and memory impairment, but protective strategies are lacking at present. It has been demonstrated that autophagy plays a critical role in HIBI, while the function of autophagy in cognitive and memory impairment induced by HIBI in neonates has not been tested. In this study, we tested the impact of autophagy on the impairment of cognitive function and memory in HIBI neonatal rats by using a Morris water maze and investigated its possible mechanisms, which were established as HIBI model by ligating the left common carotid artery in neonatal rats, followed by 2-h hypoxia. The expression of microtubule-associated protein 1 light chain 3 (LC3)-II increased in HI group 24 h after HI in neonatal rats, while Sequestosome 1 (P62/SQSTM1), phosphorylated cAMP-response element-binding protein (p-CREB) decreased (compared with the sham group, p < 0.05), which were shown in the same left hippocampus CA3 region by immunofluorescence analysis. Brain injury of neonatal rats was aggravated significantly at 7 day after HI, coinciding with the results of Morris water maze. An autophagy inhibitor, 3-methyladenine (3-MA) pretreatment significantly attenuated the increase of LC3II and the loss of P62/SQSTM1 and p-CREB, ameliorated neuronal death, and improved the results of Morris water maze. Our results demonstrate that HIBI in neonatal rats induced excessive autophagy flux, which aggravated brain injury and induced cognitive and memory impairment during adolescence. Inhibition of autophagy reversed the results partly and improved the function of spatial learning and memory by attenuating the reduction of p-CREB. The use of autophagy modulators in the immature brain would create new opportunities for protective strategies clinically in the future.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Autophagy activation involved in hypoxic‐ischemic brain injury induces cognitive and memory impairment in neonatal rats

Tian

et al. 2016

Journal of Neurochemistry

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“…Interestingly, in other reports, animals with HI injury induced on P3 showed decreases in enzymatic activity (Na + /K + ATPase) [77], as well as increases in necrotic cells and axonal disruption with prolonged astrocytic and microglial activation in deep cortical areas [78]. Studies also show reductions in cortical size with altered patterns of myelination 18 days following such injury [79].…”

Section: 4 Discussionmentioning

confidence: 97%

Behavioral and histological outcomes following neonatal HI injury in a preterm (P3) and term (P7) rodent model

Alexander

Garbus

Smith

et al. 2014

Behavioural Brain Research

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Hypoxia-ischemia (HI) occurs when blood and/or oxygen delivery to the brain is compromised. HI injuries can occur in infants born prematurely (<37 weeks gestational age) or at very low birth weight (<1500 grams), as well as in term infants with birth complications. In both preterm and term HI populations, brain injury is associated with subsequent behavioral deficits. Neonatal HI injury can be modeled in rodents (e.g., the Rice-Vannucci method, via cautery of right carotid followed by hypoxia). When this injury is induced early in life (between postnatal day (P)1–5), neuropathologies typical of human preterm HI are modeled. When injury is induced later (P7–12), neuropathologies typical of those seen in HI term infants are modeled. The current study sought to characterize the similarities/differences between outcomes following early (P3) and late (P7) HI injury in rats. Male rats with HI injury on P3 or P7, as well as sham controls, were tested on a variety of behavioral tasks in both juvenile and adult periods. Results showed that P7 HI rats displayed deficits on motor learning, rapid auditory processing (RAP), and other learning/memory tasks, as well as a reduction in volume in various neuroanatomical structures. P3 HI animals showed only transient deficits on RAP tasks in the juvenile period (but not in adulthood), yet robust deficits on a visual attention task in adulthood. P3 HI animals did not show any significant reductions in brain volume that we could detect. These data suggest that: 1) behavioral deficits following neonatal HI are task-specific depending on timing of injury; 2) P3 HI rats showed transient deficits on RAP tasks; 3) the more pervasive behavioral deficits seen following P7 HI injury were associated with substantial global tissue loss; and 4) persistent deficits in attention in P3 HI subjects might be linked to neural connectivity disturbances rather than a global loss of brain volume, given that no such pathology was found. These combined findings can be applied to our understanding of differing long-term outcomes following neonatal HI injury in premature versus term infants.

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“…An in vitro study showed that the neurons of the female subject is more resistant to ischemia when compared with male subjects 19 . Instead, Sanches et al (2013) found that 3 days old male mice were more resistant to conditions of hypoxia and ischemia 20 . The results of this study differ from previous studies which found no difference in ischemic volume between male and female rats.…”

Section: Effect Of Animal Models Sexes To Ischemic Brain Volumementioning

confidence: 99%

“…An in vitro study showed that the neurons of the female subject is more resistant to ischemia than the male subject 22 . Instead, Sanches et al (2013) found that 3 days old male rat were more resistant to hypoxia and ischemia condition 23 . Variations on BCCAO duration, reperfusion duration, strain and animal models sex could lead to different responses to ischemia condition.…”

mentioning

confidence: 97%

Effect of BCCAO Duration and Animal Models Sex on Brain Ischemic Volume After 24 Hours Reperfusion

Handayani

Nurmasitoh

Akhmad

et al. 2018

Bangladesh J Med Sci

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Abstract:Background: Literature study shows, there are several variations regarding BCCAO duration and duration of reperfusion after BCCAO that can cause cerebral ischemia. Duration of BCCAO techniques varies between 10 to 30 minutes, while the duration of reperfusion period ranging between 45 minutes to 72 hours. Differences in the duration of occlusion, duration of BCCAO reperfusion and the sex of animal model could lead to different responses to ischemia conditions. Objective. This study aims to determine whether the duration BCCAO and sex of the animal models influences the volume of cerebral ischemia after 24 hours reperfusion. Method: This study uses post-test only study group design. The subjects are 20 female and 20 male Wistar rat that being divided into 8 groups which are male rat with occlusion duration of 5 minutes, 10 minutes and 20 minute, also the female rat with occlusion duration of 5 minutes, 10 minutes, 20 minutes respectively. BCCAO occlusion then followed by 24 hour reperfusion. Rat decapitation and brain extraction are done after reperfusion. Brain tissue sliced into 2 mm size and stained with 0.05% TTC solution for 30 minutes. Ischemic brain volume are being observed using Cavalieri method. Statistical data are being analyzed using One Way Anova. Result: There are significant difference in male rat cerebral ischemia volume between 5 minutes and 10 minutes occlusion (p<0.006). Meanwhile, there are no significant difference at cerebral ischemia volume between 10 and 20 minutes occlusion group (p=0.377). There are significant differences in the volume of brain ischemia between the 5, 10 and 20 minutes ischemia group (p<0.05). Post-hoc test showed no significant differences between the male and female rat (p>0.05). Conclusion: Duration of the bilateral common carotid artery occlusion for 5 and 10 minutes affect the volume of cerebral ischemia in male rat after 24 hour reperfusion. The occlusion of bilateral common carotid artery for 5,10 and 20 minutes also affect the volume of cerebral ischemia in female rat after 24 hour reperfusion. No significant differences of cerebral ischemia volume between the sexes after 5, 10 and 20 minutes occlusion.

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Are the consequences of neonatal hypoxia–ischemia dependent on animals' sex and brain lateralization?

Cited by 32 publications

References 75 publications

Autophagy activation involved in hypoxic‐ischemic brain injury induces cognitive and memory impairment in neonatal rats

Autophagy activation involved in hypoxic‐ischemic brain injury induces cognitive and memory impairment in neonatal rats

Behavioral and histological outcomes following neonatal HI injury in a preterm (P3) and term (P7) rodent model

Effect of BCCAO Duration and Animal Models Sex on Brain Ischemic Volume After 24 Hours Reperfusion

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