Maternal separation impairs long term-potentiation in CA1-CA3 synapses and hippocampal-dependent memory in old rats

Sousa, Vasco C.; Vital, Joana; Costenla, Ana Rita; Batalha, Vânia L.; Sebastião, Ana M.; Ribeiro, Joaquim A.; Lopes, Luı́sa V.

doi:10.1016/j.neurobiolaging.2014.01.024

Cited by 76 publications

(58 citation statements)

References 48 publications

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“…Our findings demonstrate that a single exposure to sevoflurane can provoke greater long-term neuroendocrine alterations than maternal separation of equal duration. This is consistent with the reported models of maternal separations, which employ up to two weeks of daily episodes of maternal separations to induce long-term developmental abnormalities (Macrí et al, 2004; Sousa et al, 2014). Such prolonged and repeated maternal separations lead to abnormalities in adulthood, which resemble those that we observed in neonatal rats exposed to sevoflurane, e.g., exacerbated corticosterone secretion in response to stress, anxiety-like behavior in the EPM test, and reduced PPI of startle (Brunson et al, 2005; Oomen et al, 2010; Li et al, 2013).…”

Section: Discussionsupporting

confidence: 92%

Anesthesia with sevoflurane in neonatal rats: Developmental neuroendocrine abnormalities and alleviating effects of the corticosteroid and Cl− importer antagonists

Tan

Zhang

et al. 2015

Psychoneuroendocrinology

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Background 1.5 million children under 12 months of age are exposed to general anesthesia annually in the United States alone. Human and especially animal studies provide evidence that exposure to general anesthesia during the early postnatal period may lead to long-term neurocognitive abnormalities via poorly understood mechanisms. We investigated whether an immature stress response system and γ-aminobutyric acid (GABA) type A receptor activities are involved in mediating these abnormalities. Methods Sprague-Dawley rats at postnatal days 4, 5 or 6 were anesthetized with 2.1% sevoflurane for 6 hrs; maternally separated and house reared rats served as controls. Results Sevoflurane anesthesia markedly increased corticosterone levels in rat pups of both genders. In adulthood, these rats responded to stress with heightened secretion of corticosterone and a greater increase in corticosterone levels in males versus females. Only male rats, previously exposed to neonatal sevoflurane, had a higher frequency of miniature inhibitory postsynaptic currents in CA1 neurons, spent a shorter time in open arms of the elevated plus maze (EPM) and exhibited impaired prepulse inhibition (PPI) of startle. Pretreatment of male rats prior to sevoflurane with the Na+-K+-2Cl− cotransporter inhibitor, bumetanide, or the mineralocorticoid receptor antagonist, RU28318, normalized endocrine responses to stress and the EPM behavior in adulthood, while only those pretreated with bumetanide exhibited normalized PPI of startle responses. Neither bumetanide nor RU28318 altered the effect of sevoflurane on synaptic activity. Conclusions Sevoflurane-enhanced neuronal excitation and elevated corticosteroid levels at the time of anesthesia contribute to the mechanisms initiating neonatal sevoflurane-induced long-term endocrine and neurobehavioral abnormalities.

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Section: Discussionsupporting

confidence: 92%

Anesthesia with sevoflurane in neonatal rats: Developmental neuroendocrine abnormalities and alleviating effects of the corticosteroid and Cl− importer antagonists

Tan

Zhang

et al. 2015

Psychoneuroendocrinology

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“…In addition, chronic daily restraint stress induces similar effects in the rat medial PFC (Radley et al, 2004, Radley et al, 2006) and even a brief episode of uncontrollable stress causes dendritic retraction in the PFC of mice (Izquierdo et al, 2006). Moreover, experience-dependent structural plasticity and synaptic functioning in the rat hippocampus are influenced by the degree and quality of maternal care (Champagne et al, 2008, Bagot et al, 2009), which under severe circumstances can be extremely persistent throughout adulthood (Baudin et al, 2012, Sousa et al, 2014). Unlike the hippocampus and PFC, chronic stress increases spine number and dendrite complexity within limbic regions such as the nucleus accumbens (NAc) and basolateral amygdala (BLA) (Vyas et al, 2006, Christoffel et al, 2011a, Warren et al, 2014).…”

Section: Validity For Human Disordersmentioning

confidence: 99%

Pathogenesis of depression: Insights from human and rodent studies

2016

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Major depressive disorder (MDD) will affect one out of every five people in their lifetime and is the leading cause of disability worldwide. Nevertheless, mechanisms associated with the pathogenesis of MDD have yet to be completely understood and current treatments remain ineffective in a large subset of patients. In this review, we summarize the most recent discoveries and insights for which parallel findings have been obtained in human depressed subjects and rodent models of mood disorders in order to examine the potential etiology of depression. These mechanisms range from synaptic plasticity mechanisms to epigenetics and the immune system where there is strong evidence to support a functional role in the development of specific depression symptomology. Ultimately we conclude by discussing how novel therapeutic strategies targeting central and peripheral processes might ultimately aid in the development of effective new treatments for MDD and related stress disorders.

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“…These adverse effects of early life and adolescent stressors on Schaffer collateral-CA1 synaptic plasticity are evident as late as in middle-aged life, concomitant with deficits in spatial learning (Ivy et al, 2010;Sterlemann et al, 2010, Sousa et al, 2014. Mimicking the adult stressevoked effects, juvenile stress also evokes differential effects on dorsal and ventral hippocampal LTP.…”

Section: Early Life Stress and Hippocampal Ltpmentioning

confidence: 99%

The adaptive and maladaptive continuum of stress responses – a hippocampal perspective

Suri

Vaidya

2015

Reviews in the Neurosciences

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AbstractExposure to stressors elicits a spectrum of responses that span from potentially adaptive to maladaptive consequences at the structural, cellular and physiological level. These responses are particularly pronounced in the hippocampus where they also appear to influence hippocampal-dependent cognitive function and emotionality. The factors that influence the nature of stress-evoked consequences include the chronicity, severity, predictability and controllability of the stressors. In addition to adult-onset stress, early life stress also elicits a wide range of structural and functional responses, which often exhibit life-long persistence. However, the outcome of early stress exposure is often contingent on the environment experienced in adulthood, and could either aid in stress coping or could serve to enhance susceptibility to the negative consequences of adult stress. This review comprehensively examines the consequences of adult and early life stressors on the hippocampus, with a focus on their effects on neurogenesis, neuronal survival, structural and synaptic plasticity and hippocampal-dependent behaviors. Further, we discuss potential factors that may tip stress-evoked consequences from being potentially adaptive to largely maladaptive.

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Maternal separation impairs long term-potentiation in CA1-CA3 synapses and hippocampal-dependent memory in old rats

Cited by 76 publications

References 48 publications

Anesthesia with sevoflurane in neonatal rats: Developmental neuroendocrine abnormalities and alleviating effects of the corticosteroid and Cl− importer antagonists

Anesthesia with sevoflurane in neonatal rats: Developmental neuroendocrine abnormalities and alleviating effects of the corticosteroid and Cl− importer antagonists

Pathogenesis of depression: Insights from human and rodent studies

The adaptive and maladaptive continuum of stress responses – a hippocampal perspective

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