<i>Bdnf</i> DNA methylation modifications in the hippocampus and amygdala of male and female rats exposed to different caregiving environments outside the homecage

Roth, Tania L.; Matt, Stephanie; Chen, Kenneth; Blaze, Jennifer

doi:10.1002/dev.21218

Cited by 80 publications

(112 citation statements)

References 53 publications

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“…Within the amygdala, abuse-exposure is associated with decreased BDNF promoter I DNA methylation in females and decreased Bdnf promoter IV DNA methylation in males. However, in adulthood the direction of effect of abusive care on Bdnf DNA methylation in the hippocampus and amygdala suggests dynamic epigenetic changes occurring across the lifespan [117]. This phenomenon is consistent with observed biphasic responses in studies of early life adversity and expression of the Bdnf gene [118].…”

Section: Mechanistic Pathways Linking Maternal Care To Offspring Osupporting

confidence: 61%

“…In adulthood, both males and females are observed to have increased DNA methylation in Bdnf promoter I in the prefrontal cortex, but at promoter IV only abuse-exposed females are observed to have increased DNA methylation [116]. At PND 8, abuse-exposed females have increased DNA methylation of Bdnf promoter IV in the ventral hippocampus [117]. Within the amygdala, abuse-exposure is associated with decreased BDNF promoter I DNA methylation in females and decreased Bdnf promoter IV DNA methylation in males.…”

Section: Mechanistic Pathways Linking Maternal Care To Offspring Omentioning

confidence: 99%

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Influence of maternal care on the developing brain: Mechanisms, temporal dynamics and sensitive periods

Curley

Champagne

2016

Frontiers in Neuroendocrinology

205

117

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Variation in maternal care can lead to divergent developmental trajectories in offspring with implications for neuroendocrine function and behavioral phenotypes. Study of the long-term outcomes associated with mother-infant interactions suggests complex mechanisms linking the experience of variation in maternal care and these neurobiological consequences. Through integration of genetic, molecular, cellular, neuroanatomical, and neuroendocrine approaches, significant advances in our understanding of these complex pathways have been achieved. In this review, we will consider the impact of maternal care on male and female offspring development with a particular focus on the issues of timing and mechanism. Identifying the period of sensitivity to maternal care and the temporal dynamics of the molecular and neuroendocrine changes that are a consequence of maternal care represents a critical step in the study of mechanism.

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Section: Mechanistic Pathways Linking Maternal Care To Offspring Osupporting

confidence: 61%

Section: Mechanistic Pathways Linking Maternal Care To Offspring Omentioning

confidence: 99%

Influence of maternal care on the developing brain: Mechanisms, temporal dynamics and sensitive periods

Curley

Champagne

2016

Frontiers in Neuroendocrinology

205

117

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“…Epigenetic regulation at specific BDNF promoters has been correlated with impaired fear regulation and anxiety [47,48]. Early exposure to adverse events results in chromatin remodeling that influences BDNF expression in regions important for fear regulation and anxiety during adulthood [49,50]. At the genetic level, a single-nucleotide polymorphism (SNP) at BDNF codon 66 is implicated in fear regulation and anxiety [51,52].…”

Section: Introductionmentioning

confidence: 99%

Activity-dependent signaling: influence on plasticity in circuits controlling fear-related behavior

Hill

Martinowich

2016

Current Opinion in Neurobiology

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Fear regulation is impaired in anxiety and trauma-related disorders. Patients experience heightened fear expression and reduced ability to extinguish fear memories. Because fear regulation is abnormal in these disorders and extinction recapitulates current treatment strategies, understanding the underlying mechanisms is vital for developing new treatments. This is critical because although extinction-based exposure therapy is a mainstay of treatment, relapse is common. We examine recent findings describing changes in network activity and functional connectivity within limbic circuits during fear regulation, and explore how activity-dependent signaling contributes to the neural activity patterns that control fear and anxiety. We review the role of the prototypical activity-dependent molecule, brain-derived neurotrophic factor (BDNF), whose signaling has been critically linked to regulation of fear behavior.

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“…Consistent with the effect of the Val66Met SNP on neuronal development and regulated release of BDNF (Chen et al, 2006;Egan et al, 2003), a knock-in mice carrying the BDNF Val66Met SNP (BDNF Met/Met ) showed an impairment of synaptic plasticity in the mPFC and hippocampus, which might interfere with the top-down control of the amygdala, a mechanism necessary for fear regulation (Bath et al, 2012;Ninan, 2014;Ninan et al, 2010;Pattwell et al, 2012a). However, given the role of BDNF in amygdala plasticity (Rattiner et al, 2005;Rosas-Vidal et al, 2014;Roth et al, 2014), it is also plausible that the BDNF Val66Met SNP exerts a direct effect on amygdala synapses. Human BDNF Val66Met carriers continued to recruit the amygdala despite fear extinction training, suggesting an altered amygdala plasticity (Soliman et al, 2010).…”

Section: Introductionmentioning

confidence: 86%

Alteration of the Centromedial Amygdala Glutamatergic Synapses by the BDNF Val66Met Polymorphism

Galvin

Lee

2015

Neuropsychopharmacol

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Fear expression is mediated by an activation of the centromedial amygdala (CEm), the major output nucleus of the amygdaloid complex. Consistently, fear extinction is associated with an increased synaptic inhibition as well as a suppression of the excitability of the CEm neurons. However, little is known about the role of CEm glutamatergic synapses in fear regulation and anxiety-like behaviors. The BDNF Val66Met, a single-nucleotide polymorphism in the human BDNF gene, impairs fear extinction and leads to anxiety-like symptoms. To determine whether the BDNF Val66Met polymorphism affects the CEm excitatory synapses, we examined basal glutamatergic synaptic transmission and plasticity in the CEm neurons of BDNF Val66Met knock-in (BDNF(Met/Met)) mice. The BDNF Val66Met single-nucleotide polymorphism exerted an opposite effect on non-NMDA and NMDA receptor transmission with a potentiation of the former and a suppression of the latter. In addition, the decay time of NMDA currents was decreased in BDNF(Met/Met) mice, suggesting a modification of NMDA receptor subunit composition. Unlike the wild-type mice that exhibited a potentiation of non-NMDA receptor transmission following fear conditioning and a depotentiation upon fear extinction, BDNF(Met/Met) mice failed to show this experience-dependent synaptic plasticity in the CEm neurons. Our results suggest that the elevated non-NMDA receptor transmission, the suppression of NMDA receptor transmission, and an impairment of synaptic plasticity in the CEm neurons might contribute to the fear extinction deficit and increased anxiety-like symptoms in BDNF Val66Met carriers.

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Bdnf DNA methylation modifications in the hippocampus and amygdala of male and female rats exposed to different caregiving environments outside the homecage

Cited by 80 publications

References 53 publications

Influence of maternal care on the developing brain: Mechanisms, temporal dynamics and sensitive periods

Influence of maternal care on the developing brain: Mechanisms, temporal dynamics and sensitive periods

Activity-dependent signaling: influence on plasticity in circuits controlling fear-related behavior

Alteration of the Centromedial Amygdala Glutamatergic Synapses by the BDNF Val66Met Polymorphism

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