title: Morphological and functional properties of rat dentate granule cells after adrenalectomy.
abstract: After complete adrenalectomy, part of the granule cells in the dentate gyrus undergo apoptosis. Findings on morphological changes in non-apoptotic granule cells, though, have been equivocal. In the present study we examined the dendritic trees of dentate granule cells 7 days after adrenalectomy or sham operation, and tested the hypothesis that changes in dendritic trees have considerable consequences for ionic currents, as measured in the soma with whole cell recording. For the latter, we focussed on voltage-gated calcium currents, which are partly generated in distal dendrites. All cells were passively filled with a fluorescent dye via the patch pipette while recording calcium currents; subsequently the cells were three-dimensionally reconstructed with the use of a confocal microscope. In sham-operated rats, dendritic trees of cells with a soma located in the inner part of the granule cell layer (facing the hilus) were significantly smaller than trees of cells located in the outer part of the layer. Neurons from rats that had extremely low (undetectable-0.3 microg/dl) circulating levels of corticosterone displayed very small and simple dendritic trees compared to cells from adrenalectomized rats that still had residual levels of corticosterone (0.6-1.0 microg/dl), regardless of the location of their soma. Despite the observation that simple dendritic trees were seen in rats where corticosterone was extremely low, the whole cell calcium current amplitude recorded from the soma of these cells was not reduced compared to the remaining cells from adrenalectomized or sham-operated rats. Our data indicate that in the absence of corticosterone dendritic trees of dentate granule cells display atrophy but that this does not necessarily reduce ionic currents measured in the soma.
authors.affiliation: Swammerdam Institute of Life Sciences, University of Amsterdam, Kruislaan 320, 1098 SM Amsterdam, The Netherlands.
authors.forename: J
authors.initials: J
authors.lastname: Wossink
authors.forename: H
authors.initials: H
authors.lastname: Karst
authors.forename: O
authors.initials: O
authors.lastname: Mayboroda
authors.forename: M
authors.initials: M
authors.lastname: Joëls
mesh_terms: D000315:Adrenalectomy / Q000009:adverse effects; D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001284:Atrophy / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D015220:Calcium Channels / Q000378:metabolism*; D002454:Cell Differentiation / Q000502:physiology; D048429:Cell Size / Q000502:physiology; D003345:Corticosterone / Q000097:blood / Q000172:deficiency*; D003712:Dendrites / Q000378:metabolism* / Q000473:pathology; D018891:Dentate Gyrus / Q000254:growth & development* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D018613:Microscopy, Confocal; D009410:Nerve Degeneration / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D018161:Receptors, Mineralocorticoid / Q000378:metabolism*
chemical_list: D015220:Calcium Channels; D018161:Receptors, Mineralocorticoid; D003345:Corticosterone