Postnatal hypobaric hypoxia in rats impairs water maze learning and the morphology of neurones and macroglia in cortex and hippocampus

Šimonová, Zuzana; Štěrbová, Katalin; Brožek, G; Komárek, Vladimı́r; Syková, Eva

doi:10.1016/s0166-4328(02)00366-2

Cited by 44 publications

(28 citation statements)

References 31 publications

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“…The escape latencies from a spatial memory task using the Morris water maze were longer in the rats exposed to IH both upon completion of the exposure and approximately 3 mo later. These functional deficits were associated with decreased staining for neurofilament immunoreactivity, astrocytes (GFAP), and oligodendrocytes (RIP) in the hippocampus and somatosensory and motor cortices in the younger animals and only minimal changes in these regions upon reaching adulthood (30). Similar findings have been reported using other hypoxic paradigms during early postnatal life (31)(32)(33).…”

Section: Discussionsupporting

confidence: 78%

Intermittent Hypoxia during Development Induces Long-Term Alterations in Spatial Working Memory, Monoamines, and Dendritic Branching in Rat Frontal Cortex

et al. 2005

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Exposure to intermittent hypoxia (IH), such as occurs in sleep-disordered breathing, is associated with increased apoptosis in vulnerable brain regions as well as with spatial reference memory deficits in adult and developing rats. The latter are more susceptible to IH, suggesting that early exposure to IH may have long-term consequences. Rats were exposed to 14 d of room air (RA) or IH starting at postnatal d 10. Working memory was then assessed in the water maze at 4 mo of age using a delayed matching to place task in which the rats were required to locate a submerged platform hidden in a novel location on the first trial (T1 or acquisition trial), and then remember that position after a delay (T2 or test trial). Mean escape latencies and swim distances were derived and the savings (T1-T2) were used as a measure of working memory. Male but not female rats exposed to IH showed working memory deficits at both a 10-and 120-min delay (for both latency and pathlength). Additionally, Sholl analysis of Golgi-stained neurons revealed decreased dendritic branching in the frontal cortex, but not the hippocampus, of male rats exposed to IH. Norepinephrine concentrations, dopamine turnover, and tyrosine hydroxylase activity were increased similarly in males and females. However, increased dopamine concentrations were present only in the frontal cortex of female rats. In conclusion, exposure to IH during a critical developmental period is associated with long-term alterations in frontal cortical dopaminergic pathways that may underlie gender differences in neurobehavioral deficits. OSA is a highly prevalent condition that affects 2-3% of all children (1-3). It is characterized by the repetitive development of either complete or partial upper airway occlusion that leads to periodic hypoxemia and hypercapnia and to recurring arousals. In recent years, it has become apparent that OSA imposes substantial neurobehavioral morbidity (4 -6), particularly of functions pertaining to the PFC (7), and that such alterations in attention, executive, and intellectual function may not be completely reversible (8). The recent development of a rodent model, whereby IH is applied during sleep, has allowed for improved delineation of some of the potential mechanisms underlying the morbid consequences of OSA (8 -17). Furthermore, a unique period of neuronal susceptibility emerged, such that developing rats exposed to IH displayed reduced apoptosis during the immediate postnatal period but markedly enhanced neuronal cell loss between 10 and 25 d of age, compared with adult animals (18). Furthermore, exposure to IH during this period was associated with marked reductions in the ability to acquire a spatial task in the water maze and with locomotor hyperactivity in males but not in females (9). The potential irreversibility of the IH-induced effects was further suggested by Decker and colleagues (19), who reported altered dopaminergic transmission in rats exposed perinatally

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Section: Discussionsupporting

confidence: 78%

Intermittent Hypoxia during Development Induces Long-Term Alterations in Spatial Working Memory, Monoamines, and Dendritic Branching in Rat Frontal Cortex

et al. 2005

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“…Clearly, a relative sparing of brain does not necessarily indicate a lack of dysfunction, as has been documented by other researchers. 41,42 In fact, we have recently reported on dysmyelination and, more importantly, that this abnormal myelination was not reversible after reoxygenation. 35 It is also unknown if there is a difference in brain function after CIH as compared to CCH.…”

Section: Discussionmentioning

confidence: 98%

“…Gozal and colleagues have argued in the past that CIH is more deleterious in terms of brain function since there is evidence of apoptosis and memory dysfunction after CIH as compared to CCH. [42][43][44] It is possible, therefore, that CIH affects brain function more than CCH since CIH is tantamount not only to periodic decreases in O 2 but also intermittent increases in O 2 which may act as ''periodic oxidants.'' 34,45 One of the important issues in this work relates to the genesis of body and organ size reduction.…”

Section: Discussionmentioning

confidence: 99%

Differential effects of chronic intermittent and chronic constant hypoxia on postnatal growth and development

Farahani

Kanaan

Gavrialov

et al. 2007

Pediatric Pulmonology

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Summary. Exposure to chronic constant or intermittent hypoxia (CCH or CIH) may have different effects on growth and development in early life. In this work, we exposed postnatal day 2 (P2) CD1 mice to CCH or CIH (11% O 2 ) for 4 weeks and examined the effect of hypoxia on body and organ growth until P30. Regression analysis showed that weight increased in control, CCH and CIH cohorts with age with r 2 values of 0.99, 0.97, and 0.94, respectively. Between days 2 and 30, slopes were 0.93 AE 0.057, 0.76 AE 0.108, and 0.63 AE 0.061 (g/day, means AE SEM) for control, CIH, and CCH, respectively and significantly different from each other (P < 0.001). The slopes between P2 and P16 were 0.78 AE 0.012, 0.46 AE 0.002, and 0.47 AE 0.019 for control, CCH and CIH, respectively. From P16 to 30, slopes were 1.12 AE 0.033, 1.09 AE 0.143, and 0.82 AE 0.08 for control, CIH, and CCH, respectively with no significant difference from each other, suggesting a catch-up growth in the latter part of the hypoxic period. Slower weight gain resulted in a 12% and 23% lower body weight in CIH and CCH mice (P < 0.001) by P30. Lung/body ratios were 0.010, 0.015, 0.015 for control, CIH, and CCH at P30, respectively. The decrease in liver, kidney, and brain weight were greater in CCH than CIH. Smaller liver weight was shown to be due to a reduction in cell size and cell number. Liver in CIH and CCH mice showed a 5% and 10% reduction in cell size (P < 0.05) and a reduction of 28% in cell number (P < 0.001) at P30. In contrast, CCH and CIH heart weight was 13% and 33% greater than control at P30 (P < 0.05), respectively. This increase in the heart weight was due to an increase in the size of cardiomyocytes which showed an increase of 12% and 14% (P < 0.001) for CIH and CCH, respectively as compared to control. Brain weight was 0.48 and 0.46 g for CIH and CCH, respectively (95% and 92% of normal). We concluded that (a) CIH and CCH follow different body and organ growth patterns; (b) mostly with CCH, the liver and kidneys are reduced in size in a proportionate way to body size but heart, lung, and brain are either spared or increased in size compared to body weight; and (c) the decrease in liver is secondary mostly to a decrease in cell number.

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“…Rats exposed to hypoxia (8% O 2 ) for 3 h at P7 showed a deficiency in MWM and T-maze acquisition tasks (Balduini et al, 2000). Newborn rats, experiencing IH-7 km-19day (8 h/day) exposure from birth, showed an impaired learning ability at both stages of P23-32 and P100-109 (Simonova et al, 2003). The differences between our studies and these others may be related to the hypoxic mode (intensity, pattern, and duration) and the development stage when animals were exposed to hypoxia.…”

Section: Discussionmentioning

confidence: 99%

“…Many reports showed that hypoxia impaired animal's spatial learning (Shukitt-Hale et al, 1994;Almli et al, 2000;Balduini et al, 2000;Ikeda et al, 2001;Row et al, 2002;Simonova et al, 2003;Decker et al, 2003), avoidance task (Clincke and Wauquier, 1984;Viu et al, 2000), and memory consolidation (Sara, 1974;Chleide et al, 1993;Camm et al, 2001;Yonelinas et al, 2002). The study on mountain climbers by Hornbein (1989) revealed a decline in visual long-term memory after ascent.…”

Section: Introductionmentioning

confidence: 99%

Neonatal exposure to intermittent hypoxia enhances mice performance in water maze and 8-arm radial maze tasks

Zhang

Chen

et al. 2005

J. Neurobiol.

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Hypoxia has generally been reported to impair learning and memory. Here we established a hypoxia-enhanced model. Intermittent hypoxia (IH) was simulated at 2 km (16.0% O2) or 5 km (10.8% O2) in a hypobaric chamber for 4 h/day from birth to 1, 2, 3, or 4 week(s), respectively. Spatial learning and memory ability was tested in the Morris water maze (MWM) task at ages of postnatal day 36 (P36)-P40 and P85-89, respectively, and in the 8-arm maze task at P60-68. The long-term potentiation (LTP), synaptic density, and phosphorylated cAMP-responsive element-binding protein (p-CREB) level in the hippocampus were measured in mice at P36 under the IH for 4 weeks (IH-4w). The results showed that IH for 3 weeks (IH-3w) and IH-4w at 2 km significantly reduced the escape latencies of mice at P36-40 in the MWM task with significantly enhanced retention, and this spatial enhancement was further confirmed by the 8-arm maze test in mice at P60-68. The improvement in MWM induced by IH-4w at 2 km was still maintained in mice at P85-89. IH-4w at 2 or 5 km significantly increased amplitude of LTP, the number of synapse, and the p-CREB level in the hippocampus of P36 mice. These results indicated that IH (4 h/day) exposure to neonatal mice at 2 km for 3 or 4 weeks enhanced mice spatial learning and memory, which was related to the increased p-CREB, LTP, and synapses of hippocampus in this model.

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Postnatal hypobaric hypoxia in rats impairs water maze learning and the morphology of neurones and macroglia in cortex and hippocampus

Cited by 44 publications

References 31 publications

Intermittent Hypoxia during Development Induces Long-Term Alterations in Spatial Working Memory, Monoamines, and Dendritic Branching in Rat Frontal Cortex

Intermittent Hypoxia during Development Induces Long-Term Alterations in Spatial Working Memory, Monoamines, and Dendritic Branching in Rat Frontal Cortex

Differential effects of chronic intermittent and chronic constant hypoxia on postnatal growth and development

Neonatal exposure to intermittent hypoxia enhances mice performance in water maze and 8-arm radial maze tasks

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