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      Strain differences in proliferation of progenitor cells in the dentate gyrus of the adult rat and the response to fluoxetine are dependent on corticosterone

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          Abstract

          This paper investigates the role of differences in adrenal cortical function on the proliferation rate of progenitor cells in the dentate gyrus of the hippocampus in adult Sprague–Dawley (SD) and Lister-Hooded (LH) male rats. SD rats had around 60% more cells labeled with Ki67 (an index of mitosis) than LH rats under basal conditions. Bilateral adrenalectomy (ADX) increased levels in both strains, but by unequal amounts, such that post-ADX numbers of Ki67-labeled cells were similar in both strains. Daily injections of 5 mg/kg corticosterone for 7 days reduced levels to similar values in ADX rats of both strains. The activity of progenitor cells in either strain did not respond to daily i.p. injections of fluoxetine (10 mg/kg) for 14 days, but an equivalent dose administered by osmotic minipump stimulated proliferation in both by a similar proportional amount, such that strain differences persisted. S.c. implantation of a corticosterone pellet (75 mg), which flattens the diurnal rhythm in corticosterone, prevented fluoxetine delivered by minipump from activating progenitor cell mitosis in SD rats, as it had in the LH strain in a previous study. These results show that much, if not all, of the marked strain differences between SD and LH rats in progenitor cell activity, and hence rates of neurogenesis in the dentate gyrus may be ascribed to corresponding differences in adrenal cortical activity.

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          Most cited references31

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          Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus.

          Recent studies suggest that stress-induced atrophy and loss of hippocampal neurons may contribute to the pathophysiology of depression. The aim of this study was to investigate the effect of antidepressants on hippocampal neurogenesis in the adult rat, using the thymidine analog bromodeoxyuridine (BrdU) as a marker for dividing cells. Our studies demonstrate that chronic antidepressant treatment significantly increases the number of BrdU-labeled cells in the dentate gyrus and hilus of the hippocampus. Administration of several different classes of antidepressant, but not non-antidepressant, agents was found to increase BrdU-labeled cell number, indicating that this is a common and selective action of antidepressants. In addition, upregulation of the number of BrdU-labeled cells is observed after chronic, but not acute, treatment, consistent with the time course for the therapeutic action of antidepressants. Additional studies demonstrated that antidepressant treatment increases the proliferation of hippocampal cells and that these new cells mature and become neurons, as determined by triple labeling for BrdU and neuronal- or glial-specific markers. These findings raise the possibility that increased cell proliferation and increased neuronal number may be a mechanism by which antidepressant treatment overcomes the stress-induced atrophy and loss of hippocampal neurons and may contribute to the therapeutic actions of antidepressant treatment.
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            Adult neurogenesis is regulated by adrenal steroids in the dentate gyrus.

            The dentate gyrus of the rat produces new granule neurons well into adulthood. In the adult, newly born granule neurons migrate from the hilus to the granule cell layer, receive synaptic input, extend axons into the mossy fiber pathway, and express a neuronal marker. No previous studies have identified factors that regulate neuronal birth in the adult dentate gyrus. In order to determine whether glucocorticoids control neurogenesis in the adult dentate gyrus, the effects of adrenal steroid manipulations on neuronal birth were assessed using [3H]thymidine autoradiography and immunohistochemistry for the neuronal marker neuron specific enolase. Acute treatment with corticosterone produced a significant decrease in the density of [3H]thymidine-labeled cells in the hilus of the dentate gyrus. In contrast, removal of endogenous adrenal steroids stimulated increased neuronal birth; adrenalectomy resulted in a significant increase in the number of neuron specific enolase-immunoreactive [3H]thymidine labeled cells in the granule cell layer compared to sham operation. Replacement of corticosterone to adrenalectomized rats after [3H]thymidine injection did not substantially alter the increase in neurogenesis observed following adrenalectomy, even though this replacement protects cells from adrenalectomy-induced cell death. These results indicate that the rate of neurogenesis in the dentate gyrus of the adult rat is dependent upon the levels of circulating adrenal steroids.
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              Epidermal growth factor and fibroblast growth factor-2 have different effects on neural progenitors in the adult rat brain.

              Neurons and glia are generated throughout adulthood from proliferating cells in two regions of the rat brain, the subventricular zone (SVZ) and the hippocampus. This study shows that exogenous basic fibroblast growth factor (FGF-2) and epidermal growth factor (EGF) have differential and site-specific effects on progenitor cells in vivo. Both growth factors expanded the SVZ progenitor population after 2 weeks of intracerebroventricular administration, but only FGF-2 induced an increase in the number of newborn cells, most prominently neurons, in the olfactory bulb, the normal destination for neuronal progenitors migrating from the SVZ. EGF, on the other hand, reduced the total number of newborn neurons reaching the olfactory bulb and substantially enhanced the generation of astrocytes in the olfactory bulb. Moreover, EGF increased the number of newborn cells in the striatum either by migration of SVZ cells or by stimulation of local progenitor cells. No evidence of neuronal differentiation of newborn striatal cells was found by three-dimensional confocal analysis, although many of these newborn cells were associated closely with striatal neurons. The proliferation of hippocampal progenitors was not affected by either growth factor. However, EGF increased the number of newborn glia and reduced the number of newborn neurons, similar to the effects seen in the olfactory bulb. These findings may be useful for elucidating the in vivo role of growth factors in neurogenesis in the adult CNS and may aid development of neuronal replacement strategies after brain damage.
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                Author and article information

                Journal
                Neuroscience
                Neuroscience
                Neuroscience
                Elsevier Science
                0306-4522
                1873-7544
                02 December 2008
                02 December 2008
                : 157-262
                : 3
                : 677-682
                Affiliations
                Department of Physiology, Development and Neuroscience, and Cambridge Centre for Brain Repair, University of Cambridge, Downing Street, Cambridge CB2 3DY, UK
                Author notes
                [* ]Corresponding author. Tel: +44-01223-333781; fax: +44-01223-333786 jh24@ 123456cam.ac.uk
                Article
                NSC10600
                10.1016/j.neuroscience.2008.08.072
                2650100
                18930787
                5c1233fc-0b8b-46f0-bf3d-da7ce5a84946
                © 2008 Elsevier Ltd.

                This document may be redistributed and reused, subject to certain conditions.

                History
                : 21 August 2008
                Categories
                Neuropharmacology

                Neurosciences
                kpbs, potassium phosphate buffer,strain differences,neurogenesis,ct, circadian time,adx, adrenalectomized/adrenalectomy,ihc, immunohistochemistry,progenitor cells,anova, analysis of variance,corticoids,aadc, aromatic amino acid decarboxylase,hpa, hypothamalo-pituitary–adrenal,hippocampus

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