Corticosterone alters N-methyl-d-aspartate receptor subunit mRNA expression before puberty

Lee, Paul R.; Brady, Dana; Koenig, James I.

doi:10.1016/s0169-328x(03)00180-3

Cited by 79 publications

(46 citation statements)

References 45 publications

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“…Stress and/or exposure of GCs are known to potentiate the effects of concurrent neurologic insults in the hippocampus (23). Excessive GCs increase extracellular glutamate levels (43,44), calcium conductance, either voltage or ligand gated (43), alter expressions of NMDA receptor subunits (45), and reduces the uptake of glutamate by glia (46). Indeed, one previous study has shown that GCs exacerbate NMDA receptor-mediated toxicity (47).…”

Section: Discussionmentioning

confidence: 99%

Epileptogenesis Is Increased in Rats With Neonatal Isolation and Early-Life Seizure and Ameliorated by MK-801: A Long-Term MRI and Histological Study

et al. 2009

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Early-life stress has been shown to destabilize the homeostatic synaptic plasticity and compromise the developing brain to the later encountered insults. This study would determine the long-term epileptogenic effect of neonatal isolation (NI) on early-life seizure. There were five groups: normal rearing (NR) rats; NI rats; NR rats suffering from status epilepticus (SE) at P12 (NR-SE); NI-SE rats; NI-SE-MK801 rats. All adult rats were video monitored to detect behavioral seizures, examined with brain magnetic resonance imaging, and assessed for hippocampal NeuN-immunoreactive (NeuN-IR) cells. Behavioral seizures were detected in one of six NR-SE rats, all the NI-SE rats (eight of eight), and none in the NR, NI, or NI-SE-MK801 rats. High hippocampal T2 signal were only found in three of five NR-SE rats, five of six NI-SE rats, and one of five NI-SE-MK801 rats. There was a significant decrease in the number of hippocampal NeuN-IR cells in the NR-SE and NI-SE groups, compared with the NR group, and MK-801 treatment ameliorated the neuronal loss. Our results demonstrated that NI led to an increase in epileptogenesis in rat pups with early-life SE, and treatment with MK-801 could ameliorate brain injuries, indicating a critical role of N-methyl-D-aspartic acid receptor in the epileptogenic process. (Pediatr Res 66: 441-447, 2009) S eizure is one of the most common pediatric emergencies with the highest incidence in the first year of life. Animal studies have demonstrated that early-life seizures differ essentially from seizures in the adult, including the seizure behaviors, the EEG features, and their consequences. Notwithstanding the higher susceptibility to seizures, the immature brain is less vulnerable to seizure-induced injuries than the mature brain (1-5), and diverse conditions, such as the seizure severity, causes of seizure, or precipitating injuries may affect the long-term neurologic outcome (6 -9). In this regard, the circumstances under which a seizure in immature brain can cause permanent brain damage is of great interest (9,10).In most studies published to date, early-life seizures are induced in the experimental animals under normal rearing (NR) and environmental conditions. For humans, however, most early-life seizures occur in premature and sick neonates (11-13) who are hospitalized and separated from their mothers, and hence, are under stress (14,15). Emerging evidence indicates early-life stress has enduring effects on the neuroendocrine system (16,17) and destabilizes homeostatic synaptic plasticity, particularly on the hippocampal neuroplasticity (18 -22). Stress or glucocorticoids (GCs) exposure potentiates the excitotoxic effect of concurrent neurologic insults (23), for example acceleration of kindling epileptogenesis (24), and change of seizure propensity (25). We have earlier demonstrated that rat pups subjected to repetitive neonatal isolation (NI) can exacerbate cognitive deficit and anxiety-like behaviors after recurrent seizures or status epilepticus (SE) (7,9,26). However, whe...

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Section: Discussionmentioning

confidence: 99%

Epileptogenesis Is Increased in Rats With Neonatal Isolation and Early-Life Seizure and Ameliorated by MK-801: A Long-Term MRI and Histological Study

et al. 2009

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“…For example, NR1 subunit expression is increased in the hypothalamus of rats that are prone to sympathoexcitatory responses after the left coronary artery has been ligated to induce heart failure (Li et al, 2003). Similarly, chronic stress and early life adverse events have been shown to increase hypothalamic NMDA receptor subunit expression (Lee et al, 2003). The changes in composition of the NMDA receptor subunits and the receptor efficacy in the hypothalamus also have been reported for a number of other stimuli, such as light and dark cycle (Pennartz et al, 2001), aging Miller and Gore, 2002), drug abuse (Zhu et al, 1999), and chronic stress (Ziegler et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Panic-Prone State Induced in Rats with GABA Dysfunction in the Dorsomedial Hypothalamus Is Mediated by NMDA Receptors

Johnson

Shekhar

2006

J. Neurosci.

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“…In this study, prepubertal and adult animals were adrenalectomized to remove the endogenous source of corticosterone and then treated with an implant that contained 200 mg of corticosterone. They found that despite equivalent circulating plasma corticosterone levels in these implanted prepubertal and adult males, only prepubertal males showed increases in NMDA receptor subunit expression (e.g., NR2A and NR2B) in the hippocampus (Lee et al, 2003). These results suggest that the prepubertal brain may indeed be more sensitive to the effects of corticosterone compared to that of the adult.…”

Section: Behavioral and Neurobiological Consequences Of Pubertal Stressmentioning

confidence: 99%

“…Another experiment directly assessed possible differential sensitivity of the pubertal and adult brain to corticosterone (Lee, Brandy, & Koenig, 2003). In this study, prepubertal and adult animals were adrenalectomized to remove the endogenous source of corticosterone and then treated with an implant that contained 200 mg of corticosterone.…”

Section: Behavioral and Neurobiological Consequences Of Pubertal Stressmentioning

confidence: 99%

Adolescence: A central event in shaping stress reactivity

Romeo

2010

Developmental Psychobiology

267

211

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ABSTRACT:The magnitude and duration of the hormonal stress response change dramatically throughout an organism's lifespan. Although much is known about the factors that modulate stress reactivity during adulthood and how neonatal development and aging influence stress responsiveness, we know relatively little about how stress reactivity changes during the juvenile to adult transition. Recent studies in adolescent boys and girls have suggested that stress is an important factor contributing to an individual's vulnerability to various neuropsychological dysfunctions, including anxiety, depression, and drug abuse. Thus, understanding how exposure to stressors during this crucial period of development lead to negative consequences is of paramount importance. A growing body of literature indicates that pubertal organisms react differentially, both physiologically and behaviorally, to a stressor compared to adults. The purpose of this review, therefore, is to discuss the recent findings regarding the pubertal maturation of stress reactivity, while also highlighting future research directions that will aid in our understanding of stress and adolescent mental health and development. ß 2010 Wiley Periodicals, Inc. Dev Psychobiol 52: 244-253, 2010.

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Corticosterone alters N-methyl-d-aspartate receptor subunit mRNA expression before puberty

Cited by 79 publications

References 45 publications

Epileptogenesis Is Increased in Rats With Neonatal Isolation and Early-Life Seizure and Ameliorated by MK-801: A Long-Term MRI and Histological Study

Epileptogenesis Is Increased in Rats With Neonatal Isolation and Early-Life Seizure and Ameliorated by MK-801: A Long-Term MRI and Histological Study

Panic-Prone State Induced in Rats with GABA Dysfunction in the Dorsomedial Hypothalamus Is Mediated by NMDA Receptors

Adolescence: A central event in shaping stress reactivity

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