Effect of corticosteroid treatment in vitro on adrenalectomy-induced impairment of synaptic transmission in the rat dentate gyrus

Citation
Cm. Stienstra et M. Joels, Effect of corticosteroid treatment in vitro on adrenalectomy-induced impairment of synaptic transmission in the rat dentate gyrus, J NEUROENDO, 12(3), 2000, pp. 199-205
Citations number
22
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROENDOCRINOLOGY
ISSN journal
09538194 → ACNP
Volume
12
Issue
3
Year of publication
2000
Pages
199 - 205
Database
ISI
SICI code
0953-8194(200003)12:3<199:EOCTIV>2.0.ZU;2-N
Abstract
Removal of the rat adrenals results after 3 days in the appearance of apopt otic cells in the dentate gyrus. Apoptosis is accompanied by an impaired sy naptic transmission in the dentate gyrus. Substitution in vivo with a low d ose of corticosterone was found to prevent both the appearance of apoptotic cells and the functional impairment. In the present study we determined wh ether the functional normalisation after corticosterone treatment criticall y depends on prevention of apoptosis. To address this question, brain slice s from rats showing apoptosis after adrenalectomy were treated in vitro wit h the mineralocorticoid aldosterone (3 nM) or with 30 nM corticosterone, wh ich is assumed to activate both mineralo- and glucocorticoid receptors. Ste roids were briefly applied either during recording (acute effects) or sever al hours before recording (long-term effects). While the slope of the fEPSP recorded in the outer molecular layer of the dentate gyrus in response to perforant path stimulation was not affected up to 1 h after acute administr ation of the steroids, fEPSP slopes recorded 2.5-3 h after corticosterone o r aldosterone treatment were significantly increased, to the level of the s ham-operated controls. The results indicate that delayed corticosteroid eff ects through in vitro activation of mineralocorticoid receptors (MRs) are s ufficient to normalise synaptic transmission in the dentate gyrus of ADX ra ts, even in the presence of apoptotic cells. We tentatively conclude that t he impaired synaptic transmission seen after ADX is probably not primarily caused by the appearance of apoptotic cells.