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    Chronic low-dose corticosterone supplementation enhances acquired epileptogenesis in the rat amygdala kindling model of TLE

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    Author
    Taher, TR; Salzberg, M; Morris, MJ; Rees, S; O'Brien, TJ
    Date
    2005-09-01
    Source Title
    NEUROPSYCHOPHARMACOLOGY
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Salzberg, Michael; Morris, Margaret; Rees, Sandra; O'Brien, Terence; TAHER, TAUFIK RAKHMAN
    Affiliation
    Medicine, Dentistry And Health Sciences
    Metadata
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    Document Type
    Journal Article
    Citations
    Taher, T. R., Salzberg, M., Morris, M. J., Rees, S. & O'Brien, T. J. (2005). Chronic low-dose corticosterone supplementation enhances acquired epileptogenesis in the rat amygdala kindling model of TLE. NEUROPSYCHOPHARMACOLOGY, 30 (9), pp.1610-1616. https://doi.org/10.1038/sj.npp.1300709.
    Access Status
    This item is currently not available from this repository
    URI
    http://hdl.handle.net/11343/26452
    DOI
    10.1038/sj.npp.1300709
    Description

    C1 - Journal Articles Refereed

    Abstract
    Mesial temporal lobe epilepsy (MTLE) is associated with high rates of depression and anxiety. A bidirectional causal relationship has been suggested, with these psychiatric comorbidities themselves enhancing epileptogenesis, possibly via hypercortisolemia. We examined the effects on epileptogenesis of chronic supplementation with low-dose corticosterone (CS) in the electrical amygdala kindling rat model. Adult Wistar rats were ovariectomized and implanted with bipolar electrodes into the left amygdala. After 1 week recovery, one group (n=7) had CS (3 mg/100 ml--approx. 4.5 mg/kg/day) and a control group saline (n=7) added to their drinking water, and both groups underwent twice daily electrical stimulations. Rats were culled 2 weeks after reaching the fully kindled state. A stereological optical fractionator technique was used to estimate the number of CA1 pyramidal cells in the hippocampus ipsilateral to the stimulations. Fewer stimulations were required in the CS-supplemented rats than in controls to reach the fully kindled state (32 vs 81, p<0.03, Student's t-test) and the first Class V seizure (14 vs 57, p<0.05). The mean after-discharge length was greater in the CS group (p=0.03, repeated measures analysis of variance). There was no difference in the mean number of CA1 neurons (1.05 x 10(5) vs 1.04 x 10(5), p=0.98). These data demonstrate that low-dose CS enhances epileptogenesis in this model of MTLE. This provides support for the hypothesis that chronic hypercortisolemia, as a result of stress, anxiety, and/or depression, may facilitate the development and progression of epilepsy in patients with MTLE. The lack of difference in hippocampal CA1 neurons indicates that the mechanism does not primarily involve pyramidal cell loss.
    Keywords
    Central Nervous System ; Neurology and Neuromuscular Diseases; Nervous System and Disorders

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