Age-dependent effects of maternal deprivation on oxidative stress in infant rat brain

Uysal, Nazan; Gönenç, Sevil; Açıkgöz, Osman; Pekçetin, Çetin; Kayatekin, Berkant Muammer; Sönmez, Ataç; Şemin, İlgi

doi:10.1016/j.neulet.2005.04.052

Cited by 36 publications

(26 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The time points when these weight differences were first observed coincide with the end of the stress hyporesponsive period during which there are low circulating levels of stress hormones and presumable non-responsiveness to external stressors [53], [54]. However, MD during the hyporesponsive period was documented to cause alterations in adult brain function [20], [55], [56], [57], [58].…”

Section: Discussionmentioning

confidence: 98%

Prenatal Nicotine and Maternal Deprivation Stress De-Regulate the Development of CA1, CA3, and Dentate Gyrus Neurons in Hippocampus of Infant Rats

Wang

Gondré–Lewis

2013

PLoS ONE

View full text Add to dashboard Cite

Adverse experiences by the developing fetus and in early childhood are associated with profound effects on learning, emotional behavior, and cognition as a whole. In this study we investigated the effects of prenatal nicotine exposure (NIC), postnatal maternal deprivation (MD) or the combination of the two (NIC+MD) to determine if hippocampal neuron development is modulated by exposure to drugs of abuse and/or stress. Growth of rat offspring exposed to MD alone or NIC+MD was repressed until after weaning. In CA1 but not CA3 of postnatal day 14 (P14) pups, MD increased pyramidal neurons, however, in dentate gyrus (DG), decreased granule neurons. NIC had no effect on neuron number in CA1, CA3 or DG. Unexpectedly, NIC plus MD combined caused a synergistic increase in the number of CA1 or CA3 neurons. Neuron density in CA regions was unaffected by treatment, but in the DG, granule neurons had a looser packing density after NIC, MD or NIC+MD exposure. When septotemporal axes were analyzed, the synergism of stress and drug exposure in CA1 and CA3 was associated with rostral, whereas MD effects were predominantly associated with caudal neurons. TUNEL labeling suggests no active apoptosis at P14, and doublecortin positive neurons and mossy fibers were diminished in NIC+MD relative to controls. The laterality of the effect of nicotine and/or maternal deprivation in right versus left hippocampus was also analyzed and found to be insiginificant. We report for the first time that early life stressors such as postnatal MD and prenatal NIC exposure, when combined, may exhibit synergistic consequences for CA1 and CA3 pyramidal neuron development, and a potential antagonistic influence on developing DG neurons. These results suggest that early stressors may modulate neurogenesis, apoptosis, or maturation of glutamatergic neurons in the hippocampus in a region-specific manner during critical periods of neurodevelopment.

show abstract

Section: Discussionmentioning

confidence: 98%

Prenatal Nicotine and Maternal Deprivation Stress De-Regulate the Development of CA1, CA3, and Dentate Gyrus Neurons in Hippocampus of Infant Rats

Wang

Gondré–Lewis

2013

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…MS before postnatal day 14 augmented antioxidant enzyme activities and suppressed lipid peroxidation in infant rat brain. However, maternal deprivation reduced enzyme activities and increased lipid peroxidation after postnatal day 14 (Uysal et al, 2005). The difference may indicate a critical period of development in which early life stress events strongly modulate mood behavior, immune, and endocrine systems.…”

Section: Discussionmentioning

confidence: 99%

Toll-Like Receptor 4 in Paraventricular Nucleus Mediates Visceral Hypersensitivity Induced by Maternal Separation

Hui-li

Zhang

et al. 2017

Front. Pharmacol.

View full text Add to dashboard Cite

Neonatal maternal separation (MS) is a major early life stress that increases the risk of emotional disorders, visceral pain perception and other brain dysfunction. Elevation of toll-like receptor 4 (TLR4) signaling in the paraventricular nucleus (PVN) precipitates early life colorectal distension (CRD)-induced visceral hypersensitivity and pain in adulthood. The present study aimed to investigate the role of TLR4 signaling in the pathogenesis of postnatal MS-induced visceral hypersensitivity and pain during adulthood. The TLR4 gene was selectively knocked out in C57BL/10ScSn mice (Tlr4-/-). MS was developed by housing the offspring alone for 6 h daily from postnatal day 2 to day 15. Visceral hypersensitivity and pain were assessed in adulthood. Tlr4+/+, but not Tlr4-/-, mice that had experienced neonatal MS showed chronic visceral hypersensitivity and pain. TLR4 immunoreactivity was observed predominately in microglia in the PVN, and MS was associated with an increase in the expression of protein and/or mRNA levels of TLR4, corticotropin-releasing factor (CRF), CRF receptor 1 (CRFR1), tumor necrosis factor-α, and interleukin-1β in Tlr4+/+ mice. These alterations were not observed in Tlr4-/- mice. Local administration of lipopolysaccharide, a TLR4 agonist, into the lateral cerebral ventricle elicited visceral hypersensitivity and TLR4 mRNA expression in the PVN, which could be prevented by NBI-35965, an antagonist to CRFR1. The present results indicate that neonatal MS induces a sensitization and upregulation of microglial TLR4 signaling activity, which facilitates the neighboring CRF neuronal activity and, eventually, precipitates visceral hypersensitivity in adulthood.Highlights Neonatal MS does not induce chronic visceral hypersensitivity and pain in Tlr4-/- mice.Neonatal MS increases the expression of TLR4 mRNA, CRF protein and mRNA, CRFR1 protein, TNF-α protein, and IL-1β protein in Tlr4+/+ mice.TLR4 agonist LPS (i.c.v.) elicits visceral hypersensitivity and TLR4 mRNA expression in the PVN.

show abstract

“…Other consequences of maternal separation in the adult brain include elevated ACTH levels in response to a stressor (35), altered CRF binding sites in several brain areas (92,133,172), dysregulated glucocorticoid and mineralocorticoid receptor expression (92,137,179), and alterations in the serotonergic (35,162,173) and glutamatergic systems (129). In a model of repeated maternal deprivation, it has been shown that alterations of brain lipid peroxidation and the antioxidant enzymes activities are age-and sex-dependent (170). Thus, the maternal deprivation in SHRP causes a significant decrease in brain lipid peroxidation and a significant increase in GPx activity in the hippocampus, prefrontal cortex, and striatum; whereas maternal deprivation in post-SHRP causes a significant increase in brain lipid peroxidation and a significant increase in SOD activity (with no effect on GPx) in the three considered regions of the brain (170).…”

Section: Schiavone Et Almentioning

confidence: 99%

“…In a model of repeated maternal deprivation, it has been shown that alterations of brain lipid peroxidation and the antioxidant enzymes activities are age-and sex-dependent (170). Thus, the maternal deprivation in SHRP causes a significant decrease in brain lipid peroxidation and a significant increase in GPx activity in the hippocampus, prefrontal cortex, and striatum; whereas maternal deprivation in post-SHRP causes a significant increase in brain lipid peroxidation and a significant increase in SOD activity (with no effect on GPx) in the three considered regions of the brain (170). In addition, although an increase in SOD enzyme activity and lipid peroxidation in the brain of maternal-separated male rats can be observed, these parameters are stable in female rats (170), suggesting that female hormones are protective, possibly through a scavenging action of estrogens (116).…”

Section: Schiavone Et Almentioning

confidence: 99%

Severe Life Stress and Oxidative Stress in the Brain: From Animal Models to Human Pathology

Schiavone

Jaquet

Trabace

et al. 2013

Antioxidants & Redox Signaling

289

211

View full text Add to dashboard Cite

Significance: Severe life stress (SLS), as opposed to trivial everyday stress, is defined as a serious psychosocial event with the potential of causing an impacting psychological traumatism. Recent Advances: Numerous studies have attempted to understand how the central nervous system (CNS) responds to SLS. This response includes a variety of morphological and neurochemical modifications; among them, oxidative stress is almost invariably observed. Oxidative stress is defined as disequilibrium between oxidant generation and the antioxidant response. Critical Issues: In this review, we discuss how SLS leads to oxidative stress in the CNS, and how the latter impacts pathophysiological outcomes. We also critically discuss experimental methods that measure oxidative stress in the CNS. The review covers animal models and human observations. Animal models of SLS include sleep deprivation, maternal separation, and social isolation in rodents, and the establishment of hierarchy in non-human primates. In humans, SLS, which is caused by traumatic events such as child abuse, war, and divorce, is also accompanied by oxidative stress in the CNS. Future Directions: The outcome of SLS in humans ranges from resilience, over post-traumatic stress disorder, to development of chronic mental disorders. Defining the sources of oxidative stress in SLS might in the long run provide new therapeutic avenues.

show abstract

Age-dependent effects of maternal deprivation on oxidative stress in infant rat brain

Cited by 36 publications

References 20 publications

Prenatal Nicotine and Maternal Deprivation Stress De-Regulate the Development of CA1, CA3, and Dentate Gyrus Neurons in Hippocampus of Infant Rats

Prenatal Nicotine and Maternal Deprivation Stress De-Regulate the Development of CA1, CA3, and Dentate Gyrus Neurons in Hippocampus of Infant Rats

Toll-Like Receptor 4 in Paraventricular Nucleus Mediates Visceral Hypersensitivity Induced by Maternal Separation

Severe Life Stress and Oxidative Stress in the Brain: From Animal Models to Human Pathology

Contact Info

Product

Resources

About