Gender- and anxiety level-dependent effects of perinatal stress exposure on medial prefrontal cortex

Soztutar, Erdem; Çolak, Ertuğrul; Ulupinar, Emel

doi:10.1016/j.expneurol.2015.06.005

Cited by 31 publications

(25 citation statements)

References 70 publications

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“…The dendritic complexity and spine density of pyramidal neurons located in this region displayed an anxiety level-and sex-dependent reduction, especially in the stressed males. [16] Moreover, total number estimation of c-Fos (+) nuclei, indicating the neuronal activation upon stressful challenge, significantly increased in high anxious animals compared with low anxious and control groups, in both gender. These results suggest that medial PFC is a critical site of neural plasticity within the stressor controllability paradigm.…”

Section: Discussionmentioning

confidence: 91%

“…[14,15] We have recently shown that in perinatally stressed animals, dendritic complexity and spine density of pyramidal neurons in the medial PFC display anxiety level-and sex-dependent reductions. [16] Moreover, accumulating evidence suggests that a dysfunction in the glutamatergic system is evident in the prefrontal cortical neurons of MDD patients. [17] Imaging studies showed that subanesthetic doses of ketamine increased cerebral blood flow and glucose metabolic rate especially in the thalamus, frontal and parietal cortical regions.…”

Section: Anatomy • Volume 9 / Issue 3 / December 2015mentioning

confidence: 99%

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Effects of single-dose ketamine infusion on behavioral parameters and neuronal activation in the medial prefrontal cortex of juvenile rats exposed to prenatal stress

Çorumlu¹,

Aydin²,

Aydın³

et al. 2015

Anatomy

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Major depressive disorder (MDD) is the leading cause of disability worldwide. [1] This disease is characterized by loss of interest in daily activities, sadness, and feelings of tiredness, guilt or low self-worth. Since these symptoms disturb sleep, appetite and concentration skills of individuals, depression can be defined as a debilitating disor-der by its growing direct and indirect financial burden on health care spending. The estimated lifetime prevalence varies across the cultures from 3% to 16.9%. [2] Currently, there are more than twenty different antidepressant medications targeting the monoamine systems. These drugs generally work by increasing the amount of serotonin or norepinephrine in the brain. While effective in most patients, sustained remission is

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Section: Discussionmentioning

confidence: 91%

Section: Anatomy • Volume 9 / Issue 3 / December 2015mentioning

confidence: 99%

Effects of single-dose ketamine infusion on behavioral parameters and neuronal activation in the medial prefrontal cortex of juvenile rats exposed to prenatal stress

Çorumlu¹,

Aydin²,

Aydın³

et al. 2015

Anatomy

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“…Neuronal changes are highly region‐specific with the most dramatic changes occurring in limbic and prefrontal cortical areas, those involved in cognition and emotional behavior. Altered neurogenesis, neuronal density, neuronal arborization, dendritic architecture, synaptic connectivity, and myelination have all been reported in animal models of prenatal stress (Bock et al, 2015; Schuurmans and Kurrasch, 2013; Soztutar et al, 2016). Prenatal stress also disrupts sex‐specific maturation of the PFC that normally occurs in adolescence (Markham et al, 2013), thus our results could reflect not only sensitivity of the developing PFC to gestational stress but also a disruption of normative periadolescent maturation.…”

Section: Discussionmentioning

confidence: 99%

Intrauterine exposure to maternal stress alters Bdnf IV DNA methylation and telomere length in the brain of adult rat offspring

Blaze

Asok

Borrelli

et al. 2017

Intl J of Devlp Neuroscience

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DNA methylation (addition of methyl groups to cytosines) and changes in telomere length (TTAGGG repeats on the ends of chromosomes) are two molecular modifications that result from stress and could contribute to the long-term effects of intrauterine exposure to maternal stress on offspring behavior. Here, we measured methylation of DNA associated with the Brain-derived neurotrophic factor (Bdnf) gene, a gene important in development and plasticity, and telomere length in the brains of adult rat male and female offspring whose mothers were exposed to unpredictable and variable stressors throughout gestation. Males exposed to prenatal stress had greater methylation (Bdnf IV) in the medial prefrontal cortex (mPFC) compared to non-stressed male controls and stressed females. Further, prenatally-stressed animals had shorter telomeres than controls in the mPFC. Together findings indicate a long-term impact of prenatal stress on brain DNA methylation and telomere biology with relevance for behavioral and health outcomes, and contribute to a growing literature linking stress to intergenerational molecular changes.

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“…Indeed, sensory, painful, or stressful experience has been shown to change the dendritic and spine morphology in this area. A combination of prenatal stress (E14–E21) and maternal separation (P2–P21) resulted in increased c-Fos expression in the mPFC and reduced dendritic length and dendritic spines of mPFC neurons (30). A recent study has found that pyramidal neurons from the mPFC of spared nerve injury (SNI) rats are characterized by longer basal dendrites and increased spine density compared to sham-operated animals (29).…”

Section: Ontogeny Of the Central Nervous System (Cns) During The Prenmentioning

confidence: 99%

Lifetime Modulation of the Pain System via Neuroimmune and Neuroendocrine Interactions

Zouikr

Karshikoff

2017

Front. Immunol.

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Chronic pain is a debilitating condition that still is challenging both clinicians and researchers. Despite intense research, it is still not clear why some individuals develop chronic pain while others do not or how to heal this disease. In this review, we argue for a multisystem approach to understand chronic pain. Pain is not only to be viewed simply as a result of aberrant neuronal activity but also as a result of adverse early-life experiences that impact an individual’s endocrine, immune, and nervous systems and changes which in turn program the pain system. First, we give an overview of the ontogeny of the central nervous system, endocrine, and immune systems and their windows of vulnerability. Thereafter, we summarize human and animal findings from our laboratories and others that point to an important role of the endocrine and immune systems in modulating pain sensitivity. Taking “early-life history” into account, together with the past and current immunological and endocrine status of chronic pain patients, is a necessary step to understand chronic pain pathophysiology and assist clinicians in tailoring the best therapeutic approach.

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Gender- and anxiety level-dependent effects of perinatal stress exposure on medial prefrontal cortex

Cited by 31 publications

References 70 publications

Effects of single-dose ketamine infusion on behavioral parameters and neuronal activation in the medial prefrontal cortex of juvenile rats exposed to prenatal stress

Effects of single-dose ketamine infusion on behavioral parameters and neuronal activation in the medial prefrontal cortex of juvenile rats exposed to prenatal stress

Intrauterine exposure to maternal stress alters Bdnf IV DNA methylation and telomere length in the brain of adult rat offspring

Lifetime Modulation of the Pain System via Neuroimmune and Neuroendocrine Interactions

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