Corticosteroids in the brain

Joëls, Marian; Vreugdenhil, Erno

doi:10.1007/bf02802026

Cited by 59 publications

(30 citation statements)

References 136 publications

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“…So, glutamate signaling may also contribute to glucocorticoid-mediated spine plasticity (Karst et al, 2005, de Kloet et al, 2008). Activation of MR enhances excitability of hippocampal CA1 neurons whereas GR activation depresses their excitability (Joels and de Kloet, 1989, Joels and Vreugdenhil, 1998). Corticosterone, when applied to the dorsal hippocampus, depresses NMDA receptor-mediated LTP in a dose-dependent and GR-dependent fashion.…”

Section: The Neuro-endocrine Circuit Of Stress Is a Major Targetmentioning

confidence: 99%

Are BDNF and glucocorticoid activities calibrated?

2013

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One hypothesis to account for the onset and severity of neurological disorders is the loss of trophic support. Indeed, changes in the levels and activities of brain-derived neurotrophic factor (BDNF) occur in numerous neurodegenerative and neuropsychiatric diseases. A deficit promotes vulnerability whereas a gain of function facilitates recovery by enhancing survival, synapse formation and synaptic plasticity. Implementation of ‘BDNF therapies’, however, faces numerous methodological and pharmacokinetic issues. Identifying BDNF mimetics that activate the BDNF receptor or downstream targets of BDNF signaling represent an alternative approach. One mechanism that shows great promise is to study the interplay of BDNF and glucocorticoid hormones, a major class of natural steroid secreted during stress reactions and in synchrony with circadian rhythms. While small amounts of glucocorticoids support normal brain function, excess stimulation by these steroid hormones precipitate stress-related affective disorders. To date, however, because of the paucity of knowledge of underlying cellular mechanisms, deleterious effects of glucocorticoids are not prevented following extreme stress. In the present review, we will discuss the complementary roles share by BDNF and glucocorticoids in synaptic plasticity, and delineate possible signaling mechanisms mediating these effects.

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Section: The Neuro-endocrine Circuit Of Stress Is a Major Targetmentioning

confidence: 99%

Are BDNF and glucocorticoid activities calibrated?

2013

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“…There is accumulating evidence that corticosteroids, in addition to corticotropin releasing factor, play an important role in stress and the pathophysiology of anxiety disorders and depression [11,12]. It has been suggested that a disturbed HPA axis regulation may be a primary causal factor in depression.…”

Section: The Glucocorticoid Receptor and Its Role In The Central Strementioning

confidence: 99%

“…In the brain, they bind to two different intracellular receptors, the mineralocorticoid receptor (MR) and the glucocorticoid receptor (GR). MRs and GRs are co-located in brain regions that are involved in the regulation of fear and anxiety, such as hippocampus, septum, and amygdala [11,12]. Moreover, GRs are widely distributed in other parts of the brain, both in neurons and glia cells.…”

Section: The Glucocorticoid Receptor and Its Role In The Central Strementioning

confidence: 99%

“…Moreover, GRs are widely distributed in other parts of the brain, both in neurons and glia cells. Areas with particularly high GR expression are found in regions involved in the feedback regulation of the hormonal stress response, such as the paraventricular nucleus of the hypothalamus, hippocampal formation, thalamic nuclei, central amygdala, striatum, and cortical layers [11,12].…”

Section: The Glucocorticoid Receptor and Its Role In The Central Strementioning

confidence: 99%

“…As a rule of thumb the synthesis of a radiotracer (including purification and formulation) should be accomplished within three half-lives. As a consequence, 11 C and 18 F are especially suitable for radiolabeling enabling to some extent multi-step synthesis sequences.…”

Section: Introductionmentioning

confidence: 99%

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Radiolabeled Glucocorticoids as Molecular Probes for Imaging Brain Glucocorticoid Receptors by Means of Positron Emission Tomography (PET)

Steiniger¹,

Knieß²,

Bergmann³

et al. 2008

MRMC

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Over the last two decades, numerous attempts have been made to develop (11)C- and (18)F-labeled radiotracers in order to study glucocorticoid receptor (GR)-mediated abnormalities of the hypothalamus-pituitary-adrenocortical (HPA) axis function and regulation in vivo by means of positron emission tomography (PET). The present review addresses the research efforts dealing with the design, radiosynthesis and radiopharmacological evaluation of PET radiotracers for brain GR imaging. The underlying problems such as metabolic instability, insufficient blood-brain-barrier penetration and/or high non-specific binding will be discussed.

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Early life influences on life‐long patterns of behavior and health

McEwen

2003

Ment. Retard. Dev. Disabil. Res. Rev.

350

235

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The stability of a child's early life has profound effects on physical and mental health, and unstable parent-child relationships, as well as abuse, can lead to behavioral disorders and increased mortality and morbidity from a wide variety of common diseases later in life. One common consequence, namely, depressive illness, is associated with chemical imbalances in the brain and hormonal dysregulation, constituting a form of allostatic load that alters interpretations of stimuli and influences, behavioral, and hormonal responses to potentially stressful situations. The brain not only encodes information and controls the behavioral responses but it is also changed structurally by those experiences. Structural changes in the hippocampus and amygdala, which are important brain structures for cognition and emotion, are representative of what may be occurring throughout the brain as a result of allostatic load resulting from the chronic stress of a disorder such as depression. Such structural changes include dendritic debranching and hypertrophy, cell proliferation, and synaptic remodeling; they are produced by the combined overactivity of stress hormones and endogenous neurotransmitters. These mediators are normally involved in adaptation, but can also promote damage when they are dysregulated and over-active. They are very likely to be strongly biased by early life experiences. The findings from animal models thus provide a basis for understanding potential mechanisms of environmental and developmental determinants of individual differences in human stress reactivity, as well as anxiety, depression, and a host of related systemic disorders. There is an increasing amount of translational research that is beginning to tie the basic research to clinical outcomes of individuals exposed to abusive or inconsistent care-giving in early life. A major goal of studies on this important topic is to define times in development and strategies for intervening to prevent or reverse the effects of adverse early life experiences. Although prevention is clearly the preferable route, some degree of reversal of psychopathology and pathophysiology caused by early life adversity appears to be an achievable goal.

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Corticosteroids in the brain

Cited by 59 publications

References 136 publications

Are BDNF and glucocorticoid activities calibrated?

Are BDNF and glucocorticoid activities calibrated?

Radiolabeled Glucocorticoids as Molecular Probes for Imaging Brain Glucocorticoid Receptors by Means of Positron Emission Tomography (PET)

Early life influences on life‐long patterns of behavior and health

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