The adrenal gland releases
mineralocorticoids (MCs) and glucocorticoids (GCs) in response to a variety of sti
muli, including stress. Once released, these adrenal steroids
mediate a plethora of physiological responses in both the periphery and the central nervous syste
m. The collective actions of GCs in the brain are paradoxical, however, in that basal levels of GCs are essential for neuronal develop
ment, plasticity and survival, while stress levels of GCs produce neuronal loss. Aging represents another contradictory function of GCs in the brain, since lifelong exposure to GCs has been i
mplicated as a causative factor in senescent neuronal loss. In addition, glucocorticoids have also been shown to intensify neuronal da
mage in the hippoca
mpus during ische
mia and excitotoxicity through
mechanis
ms that
modulate synaptic gluta
mate concentrations. Conversely, the absence of adrenal steroids has been shown to regulate both neurogenesis and neuronal loss in the dentate gyrus of the hippoca
mpus. Evidence continues to accu
mulate which suggests that GC-induced neuronal death in all these physiological and pathophysiological settings occurs by apoptosis. Accordingly, this review will exa
mine the phar
macological, cellular and
molecular
mechanis
ms through which glucocorticoids
mediate or contribute to neuronal re
modeling and, ulti
mately, neuronal death.
Publisher: | Elsevier Science |
Language of Publication: | English |
Item Identifier: | S0891-0618(97)00031-8 |
Publication Type: | Miscellaneous |
ISSN: | 0891-0618 |
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| Footnotes: m e="footnote_1">Proceedings of the 13th International Symposium of the Journal of Steroid Biochemistry & Molecular Biology "Recent Advances in Steroid Biochemistry & Molecular Biology" Monaco, 25-28 May 1997.
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