scholarly journals Vasopressin deficiency diminishes acute and long-term consequences of maternal deprivation in male rat pups

2015 ◽  
Vol 51 ◽  
pp. 378-391 ◽  
Author(s):  
Dóra Zelena ◽  
Berhard Stocker ◽  
István Barna ◽  
Zsuzsanna E. Tóth ◽  
Gábor B. Makara
2019 ◽  
pp. S207-S217
Author(s):  
S. MURDEN ◽  
V. BORBÉLYOVÁ ◽  
Z. LAŠTŮVKA ◽  
J. MYSLIVEČEK ◽  
J. OTÁHAL ◽  
...  

Hypoxic-ischemic encephalopathy (HIE) is a neonatal condition that occurs as a consequence of perinatal asphyxia, which is caused by a number of factors, commonly via compression of the umbilical cord, placental abruption, severe meconium aspiration, congenital cardiac or pulmonary anomalies and birth trauma. Experimental studies have confirmed that male rat pups show a higher resistance to HIE treatment. Moreover, the long-term consequences of hypoxia in male are more severe in comparison to female rat pups. These sex differences can be attributed to the pathophysiology of hypoxia-ischemia, whereby studies are beginning to establish such gender-specific distinctions. The current and sole treatment for HIE is hypothermia, in which a reduction in temperature prevents long-term effects, such as cerebral palsy or seizures. However, in most cases hypothermia is not a sufficient treatment as indicated by a high mortality rate. In the present review, we discuss the gender differences within the pathophysiology of hypoxia-ischemia and delve into the role of gender in the incidence, progression and severity of the disease. Furthermore, this may result in the development of potential novel treatment approaches for targeting and preventing the long-term consequences of HIE.


2005 ◽  
Vol 30 (12) ◽  
pp. 2192-2204 ◽  
Author(s):  
Paul M Plotsky ◽  
K V Thrivikraman ◽  
Charles B Nemeroff ◽  
Christian Caldji ◽  
Shakti Sharma ◽  
...  

2012 ◽  
Vol 31 (5) ◽  
pp. 741-748 ◽  
Author(s):  
Eloïse Delamaire ◽  
Patricia Parnet ◽  
Bérengère Coupé ◽  
Christine Hoebler ◽  
Sophie Blat ◽  
...  

2008 ◽  
Vol 294 (4) ◽  
pp. R1356-R1366 ◽  
Author(s):  
Cécile Julien ◽  
Aida Bairam ◽  
Vincent Joseph

Ventilatory long-term facilitation (LTF; defined as gradual increase of minute ventilation following repeated hypoxic exposures) is well described in adult mammals and is hypothesized to be a protective mechanism against apnea. In newborns, LTF is absent during the first postnatal days, but its precise developmental pattern is unknown. Accordingly, this study describes this pattern of postnatal development. Additionally, we tested the hypothesis that chronic intermittent hypoxia (CIH) from birth alters this development. LTF was estimated in vivo using whole body plethysmography by exposing rat pups at postnatal days 1, 4, and 10 (P1, P4, and P10) to 10 brief hypoxic cycles (nadir 5% O2) and respiratory recordings during the following 2 h (recovery, 21% O2). Under these conditions, ventilatory LTF (gradual increase of minute ventilation during recovery) was clearly expressed in P10 rats but not in P1 and P4. In a second series of experiments, rat pups were exposed to CIH during the first 10 postnatal days (6 brief cyclic exposures at 5% O2 every 6 min followed by 1 h under normoxia, 24 h a day). Compared with P10 control rats, CIH enhanced hypoxic ventilatory response (estimated during the hypoxic cycles) specifically in male rat pups. Ventilatory LTF was drastically reduced in P10 rats exposed to CIH, which was associated with higher apnea frequency during recovery. We conclude that CIH from birth enhances hypoxic chemoreflex and disrupts LTF development, thus likely contributing to increase apnea frequency.


2015 ◽  
Vol 122 (1) ◽  
pp. 87-95 ◽  
Author(s):  
Levana G. Amrock ◽  
Mathew L. Starner ◽  
Kathy L. Murphy ◽  
Mark G. Baxter

Abstract Background: Neonatal exposure to general anesthetics may pose significant neurocognitive risk. Human epidemiological studies demonstrate higher rates of learning disability among children with multiple, but not single, exposures to anesthesia. The authors employ a rat model to provide a histological correlate for these population-based observations. The authors examined long-term differences in hippocampal synaptic density, mitochondrial density, and dendritic spine morphology. Methods: Twenty male rat pups (n = 5/condition) were exposed to 2.5% sevoflurane under one of four conditions: single 2-h exposure on postnatal day 7 (P7); single 6-h exposure on P7; repeated 2-h exposures on P7, P10, and P13 for a cumulative 6 h of general anesthetics; or control exposure to 30% oxygen on P7, P10, and P13. Results: Repeated exposure to general anesthetics resulted in greater synaptic loss relative to a single 2-h exposure (P < 0.001). The magnitude of synaptic loss induced by three 2-h exposures (1.977 ± 0.040 μm3 [mean ± SEM]) was more profound than that of a single 6-h exposure (2.280 ± 0.045 μm3, P = 0.022). Repeated exposures did not alter the distribution of postsynaptic density length, indicating a uniform pattern of loss across spine types. In contrast, mitochondrial toxicity was best predicted by the cumulative duration of exposure. Relative to control (0.595 ± 0.017), both repeated 2-h exposures (0.479 ± 0.015) and a single 6-h exposure (0.488 ± 0.013) were associated with equivalent reductions in the fraction of presynaptic terminals containing mitochondria (P < 0.001). Conclusion: This suggests a “threshold effect” for general anesthetic–induced neurotoxicity, whereby even brief exposures induce long-lasting alterations in neuronal circuitry and sensitize surviving synapses to subsequent loss.


2016 ◽  
Vol 26 ◽  
pp. S712-S713 ◽  
Author(s):  
I. Sukhanova ◽  
D. Khukhareva ◽  
E. Sebentsova ◽  
M. Vyssokikh ◽  
N. Levitskaya

2012 ◽  
Vol 62 (3) ◽  
pp. 1332-1341 ◽  
Author(s):  
Alvaro Llorente-Berzal ◽  
Virginia Mela ◽  
Erika Borcel ◽  
Manuel Valero ◽  
Meritxell López-Gallardo ◽  
...  

2020 ◽  
Author(s):  
Gabriel Olaiya Omotoso ◽  
Fatimah Adeola Abdulsalam ◽  
Nafisat Yetunde Mutholib ◽  
Abdulkabir Bature ◽  
Ismail Temitayo Gbadamosi

ABSTRACTMaternal deprivation (MD) during early life development has been documented to culminate in long-term alterations in brain function and behavioural manifestations that mimic schizophrenia. This study elucidated the putative neuroprotective roles of vitamin B complex in MD-induced behavioural and neurochemical modifications in hippocampus and prefrontal cortex of Wistar rats. Rat pups were maternally deprived on postnatal day 9 for 24 hours and then treated with or without vitamin B complex for 15 days while a control group was undisturbed during the experimental period. The rats were then subjected to behavioural paradigms to measure memory indices and anxiety levels. The rats were sacrificed to obtain the PFC and hippocampus for histomorphological and biochemical analysis. Behavioural analysis of the animals revealed that MD induced a declination in long- and short-term memory in addition to anxiety-like behaviour in the open field test. Cortico-hippocampal histomorphology of these animals showed an increased astrocytic density and chromatolysis, which were accompanied by reduced levels of superoxide dismutase and catalase enzymes. Vitamin B complex mitigated MD-induced behavioural decline, histomorphological perturbation and oxidative stress by enhancing the intrinsic antioxidant defence, thereby culminating in nootropic behaviour and reduced anxiety. In conclusion, we confirmed the hypothesis that vitamin B complex is neuroprotective against neuropathological alterations induced by maternal deprivation.


Sign in / Sign up

Export Citation Format

Share Document