oligodendrocytes and glucocorticoid receptors

Oligodendrocytes and Glucocorticoid Receptors

There is an important link between high levels of cortisol and damage to oligodendrocytes.

In the most general terms of association, some of the glucocorticoid receptors whose negative feedback help control high levels of cortisol are in the white matter of the brain. Damage to oligodendrocytes affect these receptors; so do high levels of cortisol. There is also a glutamate toxicity- oligodendrocyte-glucocorticoid connection.

Again, as an overview, two glutamate related drugs, lamictal and topiramate are effective. Another drug, Seroquel/quetiapine, lowers cortisol levels and positively affects oligodendrocytes. These are addressed in other blogs, but I hope to get into more about the specifics and the apparent cause and effects later.

lead and later toxic cortisol responsiveness

Here is an interesting connection between a toxin (lead) and its human effects on on abnormally high cortisol reactions to stress:

Environmental Health Perspectives Volume 116, Number 2, February 2008

Research | Children's Health

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Low-Level Prenatal and Postnatal Blood Lead Exposure and Adrenocortical Responses to Acute Stress in Children

Brooks B. Gump,¹ Paul Stewart,¹ Jacki Reihman,¹ Ed Lonky,¹ Tom Darvill,¹ Patrick J. Parsons,^2,3 and Douglas A. Granger⁴

¹Department of Psychology, State University of New York College at Oswego, Oswego, New York, USA; ²Trace Elements Laboratory, Wadsworth Center, New York State Department of Health, Albany, New York, USA; ³Department of Environmental Health Sciences, School of Public Health, The University at Albany, Albany, New York, USA; ⁴Behavioral Endocrinology Laboratory, Department of Biobehavioral Health, Pennsylvania State University, State College, Pennsylvania, USA

• Introduction
• Methods
• Results
• Discussion

Abstract
Background: A few recent studies have demonstrated heightened hypothalamic–pituitary–adrenal (HPA) axis reactivity to acute stress in animals exposed to heavy metal contaminants, particularly lead. However, Pb-induced dysregulation of the HPA axis has not yet been studied in humans.

Objective: In this study, we examined children's cortisol response to acute stress (the glucocorticoid product of HPA activation) in relation to low-level prenatal and postnatal Pb exposure.

Methods: Children's prenatal blood Pb levels were determined from cord blood specimens, and postnatal lead levels were abstracted from pediatrician and state records. Children's adrenocortical responses to an acute stressor were measured using assays of salivary cortisol before and after administration of a standard cold pressor task.

Results: Pb exposure was not associated with initial salivary cortisol levels. After an acute stressor, however, increasing prenatal and postnatal blood Pb levels were independently associated with significantly heightened salivary cortisol responses.

Conclusions: Our results suggest that relatively low prenatal and postnatal blood lead levels—notably those below the 10 µg/dL blood lead level identified by the Centers for Disease Control and Prevention for public health purposes—can alter children's adrenocortical responses to acute stress. The behavioral and health consequences of this Pb-induced HPA dysregulation in children have yet to be determined.

EFFECTS OF HEXACHLOROPHENE EXPOSURE

HOW DOES EXPOSURE TO HEXACHLOROPHENE CAUSE LATER EFFECTS OF HIGH LEVELS OF THE STRESS HORMONE, CORTISOL?

I hope to be adding to this soon.