Corticosterone shifts different forms of synaptic potentiation in opposite directions

Krugers, Harmen J.; Alfarez, D.N.; Karst, H.; Parashkouhi, K.; Gemert, Neeltje G. van; Joëls, Marian

doi:10.1002/hipo.20092

Cited by 86 publications

(70 citation statements)

References 51 publications

(77 reference statements)

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“…Water depth was 40 cm, and temperature was maintained at 23 Ϯ 1°C. Stress exposure was always commenced at 9:00 A.M., when the plasma corticosterone levels are low (Finn et al, 2003, Krugers et al, 2005.…”

Section: Methodsmentioning

confidence: 99%

Differential Modulation of Long-Term Depression by Acute Stress in the Rat Dorsal and Ventral Hippocampus

Maggio

Segal²

2009

Journal of Neuroscience

112

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The ventral hippocampus (VH) was recently shown to express lower-magnitude long-term potentiation (LTP) than the dorsal hippocampus (DH). An exposure to acute stress reversed this difference, and VH slices from stressed rats expressed larger LTP than controls, whereas LTP in the DH was suppressed by stress. We have now used long-term depression (LTD)-generating trains of stimulation to examine whether this differential LTP reflects a genuine difference in synaptic modifiability between the two sectors of the hippocampus. Surprisingly, slices of DH and VH express similar magnitudes of LTD. However, while prior stress enhanced LTD in the DH, it actually converted LTD to slow-onset, robust LTP in the VH. These two effects of stress on LTD were blocked by glucocorticosterone receptor (GR) and mineralocorticosterone receptor (MR) antagonists, respectively. Acute exposure of slices to a GR agonist dexamethasone facilitated LTD in slices of both DH and VH, while activation of MRs by aldosterone converted LTD to LTP in both regions. Thus, differential activation of the two species of corticosterone receptors determines the ability of the two sectors of the hippocampus to undergo plastic changes in response to LTD-inducing stimulation.

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Section: Methodsmentioning

confidence: 99%

Differential Modulation of Long-Term Depression by Acute Stress in the Rat Dorsal and Ventral Hippocampus

Maggio

Segal²

2009

Journal of Neuroscience

112

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“…To assess the effects of GR or MR activation on neuronal activity of AHA GABAergic neurons, endogenous corticosterone was removed by bilateral ADX, and GR or MR was activated experimentally by in vitro slice incubation according to Krugers et al [20]. One hour after the slice preparation, as described above, the brains from the ADX mice were treated for 20-min at 31 o C with one of the following: 1) vehicle (0.1% DMSO in ACSF, control group), 2) corticosterone (100 nM in ACSF, CORT group), 3) 100 nM corticosterone plus a GR antagonist, RU486 (500 nM in ACSF, MR-dominant group), or 4) 100 nM corticosterone plus an MR antagonist, spironolactone (100 nM in ACSF, GR-dominant group).…”

Section: Selective Activation Of Corticosteroid Receptors and Electromentioning

confidence: 99%

Direct Corticosteroid Modulation of GABAergic Neurons in the Anterior Hypothalamic Area of GAD65-eGFP Mice

Shin¹,

Han²,

Lee³

et al. 2011

Korean J Physiol Pharmacol

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Corticosterone is known to modulate GABAergic synaptic transmission in the hypothalamic paraventricular nucleus. However, the underlying receptor mechanisms are largely unknown. In the anterior hypothalamic area (AHA), the sympathoinhibitory center that project GABAergic neurons onto the PVN, we examined the expression of glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) of GABAergic neurons using intact GAD65-eGFP transgenic mice, and the effects of corticosterone on the burst firing using adrenalectomized transgenic mice. GR or MR immunoreactivity was detected from the subpopulations of GABAergic neurons in the AHA. The AHA GABAergic neurons expressed mRNA of GR (42%), MR (38%) or both (8%). In addition, in brain slices incubated with corticosterone together with RU486 (MR-dominant group), the proportion of neurons showing a burst firing pattern was significantly higher than those in the slices incubated with vehicle, corticosterone, or corticosterone with spironolactone (GR-dominant group; 64 vs. 11∼ 14% , p＜ 0.01 by χ 2 -test). Taken together, the results show that the corticosteroid receptors are expressed on the GABAergic neurons in the AHA, and can mediate the corticosteroid-induced plasticity in the firing pattern of these neurons. This study newly provides the experimental evidence for the direct glucocorticoid modulation of GABAergic neurons in the AHA in the vicinity of the PVN.

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“…Acute stress can promote hippocampus-mediated cognitive function and synaptic transmission [100,149,78,71,21,68,81 but see 151]. The short-term effects of this facilitation may be mediated by glucocorticoids [44,81]. Additionally, local release of CRH from hippocampal neurons during acute stress [37] may prime long-term potentiation [20].…”

Section: Recognized Effects Of Stress On Hippocampal Integrity and Fumentioning

confidence: 99%

Hippocampal neuroplasticity induced by early-life stress: Functional and molecular aspects

Fenoglio¹,

Brunson²,

Baram³

2006

Frontiers in Neuroendocrinology

192

138

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Whereas genetic factors contribute crucially to brain function, early-life events, including stress, exert long-lasting influence on neuronal function. Here, we focus on the hippocampus as the target of these early-life events because of its crucial role in learning and memory. Using a novel immaturerodent model, we describe the deleterious consequences of chronic early-life 'psychological' stress on hippocampus-dependent cognitive tasks. We review the cellular mechanisms involved and discuss the roles of stress-mediating molecules, including corticotropin releasing hormone, in the process by which stress impacts the structure and function of hippocampal neurons. KeywordsNeonatal; Rat; Human; Stress; Memory; Hippocampus; Corticotropin releasing hormone; CRF; Hypothalamic pituitary adrenal axis; Neuroplasticity Early-life events interact with genetic factors to influence hippocampal function long-termBrain function and dysfunction throughout life are determined by the interaction of genetic factors with 'acquired' environmental events, signals and stimuli [100]. Events that occur early in life are capable of exerting effects that persist throughout adulthood. Here, we focus on the hippocampus as the target of these early-life events because of its crucial role in learning, memory storage and retrieval, and general cognitive function [105,41,65]. Indeed, early-life events, via complex interactions with genetic factors [106,120], have been suspected to be a major determinant of smaller hippocampal volume and long-term cognitive dysfunction in preterm infants [111,17] and may play a role in certain affective and dementing disorders in the adult and aging human [100,26,120]. This review focuses on the mechanisms by which certain early-life events influence populations of hippocampal neurons acutely, and impact the function and integrity of the hippocampus long-term. Studying early-life stress may be used to probe the molecular mechanisms involved in experience-evoked hippocampal neuroplasticityStress may provide a salient example of early-life experience that might exert long-lasting influence on the brain, because (1) over 50% of the world's children are exposed to stress [139] and (2) evidence from both human and animal studies suggests that early-life stress has profound effects on cognitive function and emotional health.Stress has been shown to influence the hippocampus in a number of important ways. Whereas acute mild stress rapidly enhances synaptic efficacy and learning and memory processes [131,45,91,123], chronic or severe activation of the stress response early in life has been shown to be potentially injurious in both humans [6,120,147] and experimental animals [120,31]. For example, severe childhood psychological stress (neglect and abuse) correlates with a higher incidence of learning disabilities later in life, including those learning and memory functions requiring an intact hippocampus [121,50]. Further, MRI studies have suggested that adults subjected to abuse (a measure of chronic stress) ...

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Corticosterone shifts different forms of synaptic potentiation in opposite directions

Cited by 86 publications

References 51 publications

Differential Modulation of Long-Term Depression by Acute Stress in the Rat Dorsal and Ventral Hippocampus

Differential Modulation of Long-Term Depression by Acute Stress in the Rat Dorsal and Ventral Hippocampus

Direct Corticosteroid Modulation of GABAergic Neurons in the Anterior Hypothalamic Area of GAD65-eGFP Mice

Hippocampal neuroplasticity induced by early-life stress: Functional and molecular aspects

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