Disruptions of the mother–infant relationship and stress-related behaviours: Altered corticosterone secretion does not explain everything

Faturi, Claudia B.; Tiba, Paula Ayako; Kawakami, Suzi Emiko; Catallani, Bruna; Kerstens, Marieke; Suchecki, Deborah

doi:10.1016/j.neubiorev.2009.09.002

Cited by 72 publications

(61 citation statements)

References 183 publications

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“…Maternal separation alters the HPA axis, with reports of either hypersensitivity marked by elevated basal and stress-induced blood corticosterone measured later in life (Higley et al, 1991;Plotsky and Meaney, 1993;Vazquez et al, 2005a) or hyposensitivity marked by lower basal and stress-induced blood corticosterone levels (Greisen et al, 2005;Kim et al, 2005;Roman et al, 2006); however, these latter studies assayed blood after testing animals in different behavioral tasks such as the elevated plus maze. Despite these discrepant findings, prolonged maternal separation blunts the negative feedback of glucocorticoids on the HPA axis (Ladd et al, 2004) and produces a constellation of behavioral changes reflecting increased anxiety and depressive symptoms Faturi et al, 2010). Even more subtle early life stress, such as being reared by a mother who engages in low levels of licking and grooming her offspring, engenders hypersensitivity and slower negative feedback of the HPA axis (Liu et al, 1997), thus attesting to the long-lasting influence of early life mother-infant interactions.…”

Section: B Social Influencesmentioning

confidence: 99%

Individual Differences and Social Influences on the Neurobehavioral Pharmacology of Abused Drugs

2013

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Section: B Social Influencesmentioning

confidence: 99%

Individual Differences and Social Influences on the Neurobehavioral Pharmacology of Abused Drugs

2013

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“…However, the HPA system upset does not explain all stress-induced alterations by itself (Kehoe & Blass 1986, Pieretti et al 1991, Ploj et al 1999, Coccurello et al 2009, Faturi et al 2010. The involvement of concurrent hormonal/neurohumoral mechanisms other than ACTH-glucocorticoids was also hypothesized to further elucidate the pathogenesis of stress-derived diseases, but clear demonstration for the identity and for the pathogenetic role of other substances (e.g.…”

Section: Diabetes-related Stress Mechanismsmentioning

confidence: 99%

“…Investigations focused chiefly the role played by genetic, endocrine, alimentary, and environmental mechanisms (see for example Andrikopoulos (2010), Faturi et al (2010), DIAGRAM Consortium (2012) and Gilbert & Liu (2012)). We underline that stressful procedures applied in pediatric ages also appear of great importance for the triggering of type 2 diabetes in adult humans.…”

Section: Introductionmentioning

confidence: 99%

Enhanced brain performance in mice following postnatal stress

Loizzo

Spampinato

Campana

et al. 2012

Journal of Endocrinology

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The double postnatal stress model (brief maternal separation plus sham injection daily applied from birth to weaning) induces metabolic alterations similar to type 2 diabetes in young-adult male mice. We verify whether 1) the stress also induces brain metabolic-functional alterations connected to diabetes and 2) different alterations are modulated selectively by two stress-damaged endogenous systems (opioid-and/or ACTH-corticosteroid-linked). Here, diabetes-like metabolic plus neurophysiologicneurometabolic parameters are studied in adult mice following postnatal stress and drug treatment. Surprisingly, together with 'classic' diabetes-like alterations, the stress model induces in young-adult mice significantly enhanced brain neurometabolic-neurophysiologic performances, consisting of decreased latency to flash-visual evoked potentials (Kw8%); increased level (Cw40%) and reduced latency (Kw30%) of NAD(P)H autofluorescence postsynaptic signals following electric stimuli; enhanced passive avoidance learning (Cw135% latency); and enhanced brain-derived neurotrophic factor level (Cw70%). Postnatal treatment with the opioid receptor antagonist naloxone prevents some alterations, moreover the treatment with antisense (AS; AS vs proopiomelanocortin mRNA) draws all parameters to control levels, thus showing that some alterations are bound to endogenous opioid-system hyper-functioning, while others depend on ACTHcorticosterone system hyper-functioning. Our stress model induces diabetes-like metabolic alterations coupled to enhanced brain neurometabolic-neurophysiologic performances. Taken all together, these findings are compatible with an 'enduring acute-stress' reaction, which puts mice in favorable survival situations vs controls. However, prolonged hormonal-metabolic imbalances are expected to also produce diabetes-like complications at later ages in stressed mice.

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“…A single 24-hr episode of early maternal deprivation (MD) in rodents has been widely used to model severe early-life stress such as child abuse and neglect. This model was shown to promote behavioral impairments with disturbances in stress responsiveness that resemble anxiety-, depressive-, psychotic-, and addictive-like symptoms (Faturi et al, 2010;Gruss et al, 2008;Kember et al, 2012;Marco et al, 2009;Nishi et al, 2014;Roceri et al, 2002). During MD, the hypothalamic-pituitary-adrenal stress response is persistently upregulated and the ability of MD animals to cope with stressful situations is significantly diminished, with symptoms evident from adolescence and into adulthood (Marco et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Histone Deacetylase Inhibition Rescues Maternal Deprivation-Induced GABAergic Metaplasticity through Restoration of AKAP Signaling

Authement

Kodangattil

Gouty

et al. 2015

Neuron

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Adverse early-life experiences such as child neglect and abuse increase the risk of developing addiction and stress-related disorders through alterations in motivational systems including the mesolimbic dopamine (DA) pathway. Here we investigated whether a severe early-life stress (i.e., maternal deprivation, MD) promotes DA dysregulation through an epigenetic impairment of synaptic plasticity within ventral tegmental area (VTA) DA neurons. Using a single 24-hr episode of MD and whole-cell patch clamp recording in rat midbrain slices, we show that MD selectively induces long-term depression (LTD) and shifts spike timing-dependent plasticity (STDP) toward LTD at GABAergic synapses onto VTA DA neurons through epigenetic modifications of postsynaptic scaffolding A-kinase anchoring protein 79/150 (AKAP79/150) signaling. Histone deacetylase (HDAC) inhibition rescues GABAergic metaplasticity and normalizes AKAP signaling in MD animals. MD-induced reversible HDAC-mediated GABAergic dysfunction within the VTA may be a mechanistic link for increased propensity to mental health disorders following MD.

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Disruptions of the mother–infant relationship and stress-related behaviours: Altered corticosterone secretion does not explain everything

Cited by 72 publications

References 183 publications

Individual Differences and Social Influences on the Neurobehavioral Pharmacology of Abused Drugs

Individual Differences and Social Influences on the Neurobehavioral Pharmacology of Abused Drugs

Enhanced brain performance in mice following postnatal stress

Histone Deacetylase Inhibition Rescues Maternal Deprivation-Induced GABAergic Metaplasticity through Restoration of AKAP Signaling

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