Abstract:
:Corticosteroids, released from the adrenal gland in response to stress, bind to receptors that act as transcription factors to alter gene expression and, subsequently, protein synthesis. Using [(35)S]-methionine-cysteine incorporation to measure protein synthesis in hippocampal slices incubated under ischemic conditions, synthesis of 60 kDa and 78 kDa proteins decreases 4 hr after in vivo administration of corticosterone to rats. The former protein has been identified by immunoblotting and immunoprecipitation to be the proto-oncogene, pp60(c-src). In the absence of prior glucocorticoid administration, ischemic conditions increase the amount of immunoreactive pp60(c-src) in membranes of hippocampal slices. Chronic exposure to elevated titers of glucocorticoids has been demonstrated to result in cell loss as well as in reduced neuronal plasticity and regeneration. Given the involvement of pp60(c-src) in synaptic plasticity and cell growth, glucocorticoid-mediated reduction in its synthesis is a potential molecular marker for stress-induced alterations in brain function.
journal_name
J Neurosci Resjournal_title
Journal of neuroscience researchauthors
Barr CS,Dokas LAdoi
10.1002/jnr.1159keywords:
subject
Has Abstractpub_date
2001-08-15 00:00:00pages
340-5issue
4eissn
0360-4012issn
1097-4547journal_volume
65pub_type
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