Neuronal and astroglial alterations in the hippocampus of a mouse model for type 1 diabetes

Revsin, Yanina; Saravia, Flavia; Roig, Paulina; Lima, Analı́a; Kloet, E. Ronald de; Homo‐Delarche, Françoise; Nicola, Alejandro F. De

doi:10.1016/j.brainres.2004.12.032

Cited by 85 publications

(67 citation statements)

References 75 publications

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“…Our result is similar to previous studies Baydas et al, 2003a;Revsin et al;Baydas et al, 2003b). Revsin et al study showed that one month after STZ treatment, the number of astrocytes significantly increased in the STZtreated group as compared to the vehicle treated group.…”

Section: Discussionsupporting

confidence: 93%

“…A variety of functional and morphological alterations in the central nervous system can be caused by Diabetes mellitus (Biessels et al, 1994). These changes include abnormal expression of hypothalamic neuropeptides, astrogliosis in the hippocampus (Saravia et al, 2002), decreased synaptic plasticity in the hippocampus, neurotoxicity, and changes in glutamate neurotransmission (Revsin et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…Some researches have indicated that diabetes led to astroglial alterations as increasing of number of astrocytes Baydas et al, 2003a;Revsin et al;Baydas et al, 2003b).…”

Section: Introductionmentioning

confidence: 99%

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Alteration of Dentate Gyrus Astrocytes in Diabetic Rats: Protective Role of Urtica dioica

et al. 2011

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GOLALIPOUR, M. J.; GHAFARI, S.; LATIFIMOGHADAM, M. H. & KABOLI, S.Alteration of dentate gyrus astrocytes in diabetic rats: Protective role of Urtica dioica. Int. J. Morphol., 29(4):1307-1312, 2011. SUMMARY:Diabetes mellitus can cause astrocytes alterations in the central nervous system. Urtica dioica (Nettle) is among several species listed for their use against diabetes in folk medicine. Therefore, this study was done to evaluate the protective effect of Urtica dioica on astrocytes density of the dentate gyrus in STZ induced diabetic rats. In this experimental study, 21 male albino Wistar rats were randomly allocated equally into normal, diabetic and protective (nettle treated diabetic) groups. Hyperglycemia was induced by streptozotocin (80 mg/kg) in the animals of diabetic and treatment groups. Before induction of diabetes in animals, animals in protective group received hydroalcoholic extract of Urtica dioica (100 mg/kg/BW /day) for five days intraperitoneally. Four weeks after induction of diabetes, animals were sacrificed and coronal sections were taken from the dorsal hippocampal formation of the right cerebral hemispheres and stained with PTAH stain. The area densities of the astrocytes were measured and compared in the three groups (p < 0.05). The number of astrocytes in DG area of controls was 17.72±6.7. The density of astrocytes increased in diabetic (24.26±9.5) in comparison with controls. The density in the nettle treated rats (23.17±5.8) was lower than diabetic rats. This study showed that the administration of U. dioica extract before induction of diabetes can not significantly help compensate for astrocytes in the dentate gyrus of treated rats.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

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Alteration of Dentate Gyrus Astrocytes in Diabetic Rats: Protective Role of Urtica dioica

et al. 2011

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“…Indeed, uncontrolled diabetes is known to produce signs of hippocampal pathology, which proceeds together with changes in other brain structures such as hypothalamus and cerebral cortex. The hippocampus of the diabetic mice exhibited increased neuronal activation, signs of oxidative stress, and astrogliosis [72][73][74]. Cognitive deficits were also observed in the hippocampus-dependent novel object-placement recognition task [75], in which mild hippocampal alterations can be tested under conditions of novelty exposure.…”

Section: Normalization Of Hippocampal Alterations During Diabetes Melmentioning

confidence: 99%

Regulation of Structural Plasticity and Neurogenesis during Stress and Diabetes; Protective Effects of Glucocorticoid Receptor Antagonists

Lucassen

Fitzsimons

Vreugdenhil

et al. 2011

Hormones in Neurodegeneration, Neuroprotection, and Neurogenesis

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Regulation of structural plasticity and neurogenesis during stress and diabetes; protective effects of glucocorticoid receptor antagonists Lucassen, P.J.; Fitzsimons, C.P.; Vreugdenhil, E.; Hu, P.; Oomen, C.A.; Revsin, Y.; Joëls, M.; de Kloet, E.R. Published in:Hormones in neurodegeneration, neuroprotection, and neurogenesis DOI:10.1002/9783527633968.ch6 Link to publication Citation for published version (APA):Lucassen, P. J., Fitzsimons, C. P., Vreugdenhil, E., Hu, P., Oomen, C., Revsin, Y., ... de Kloet, E. R. (2011). Regulation of structural plasticity and neurogenesis during stress and diabetes; protective effects of glucocorticoid receptor antagonists. In A. G. Gravanis, & S. H. Mellon (Eds.), Hormones in neurodegeneration, neuroprotection, and neurogenesis (pp. 103-120). Weinheim: Wiley-VCH. DOI: 10.1002/9783527633968.ch6 General rightsIt is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. Paul J. Lucassen, Carlos P. Fitzsimons, Erno Vreugdenhil, Pu Hu, Charlotte Oomen, Yanina Revsin, Marian Joëls, and E. Ron• De Kloet Q1 In this chapter, we will review changes in structural plasticity of the adult hippocampus during stress and exposure to glucocorticoids (GCs). We further discuss the protective and normalizing role of glucocorticoid receptor (GR) antagonist treatment under these conditions and its implications for disorders such as depression and diabetes mellitus. The Stress ResponseStress represents an old, yet essential alarm system for an organism. Whenever a discrepancy occurs between an organism's expectations and the reality it encounters, stress systems are activated; particularly when it involves a threat to, or disturbance of its homeostasis, well being, or health. Loss of control, or unpredictability when faced with predator threat in animals, or psychosocial demands in humans, can all produce stress signals. The same holds true for perturbations of a more physical or biological nature, such as energy crises, injury, or inflammation. Upon exposure to a stressor, various sensory and cognitive signals converge to activate a stress response that triggers several adaptive processes in the body and brain which aim to promote restoration of homeostasis.In mammals, Selye [1] noted that the effect of stressors develops in a stereotypic manner. The first phase largely...

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“…By induction of apoptosis (Jackson-Guilford et al; Li et al, 2002aLi et al, , 2002bAhmadpour & Haghir, 2011;Ahmadpour et al, 2008Ahmadpour et al, , 2010Britton et al, 2003;Gao & Gao, 2007;Grillo et al, 2005;Li et al, 2002aLi et al, , 2002bRevsin et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Hippocampal Neuronal Apoptosis in Rat Offspring Due to Gestational Diabetes

et al. 2016

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GHAFARI, S.; ASADI, E.; SHABANI, R. & GOLALIPOUR, M. J.Hippocampal neuronal apoptosis in rat offspring due to gestational diabetes. Int. J. Morphol., 34(1):205-211, 2016. SUMMARY:Gestational diabetes mellitus (GDM) defined as impaired glucose tolerance affects approximately 6 % of all pregnant women who have never before had diabetes, but who do have high blood glucose levels during pregnancy. This study was done to evaluate the apoptosis in the neuronal cells in the CA1, CA2 and CA3 subfields of hippocampus and dentate gyrus in offspring of gestational diabetes at the 7, 21 and 28 d in postnatal rats. Thirty Wistar rat dams were randomly allocated in control and diabetic group. Dams in diabetic group were received 40 mg/kg/BW of streptozotocin at the first day of gestation and control groups received an equivalent volume normal saline injection intraperitoneally (IP). Six offspring of GDM and control dams, at the 7, 21, 28 postnatal day were randomly were sacrificed quickly with anesthesia. The coronal sections of brain serially collected. The apoptosis neurons were evaluated with TUNEL Assay. In the CA1, the number of apoptotic cells in 7, 21 and 28 d of postnatal life were significantly increased in GDM compared to controls (P<0.001). In the CA2, CA3 the number of apoptotic cells in 7, 21 and 28 d age-old offspring were significantly increased in GDM compared to controls (P<0.001). In the dentate gyrus, the number of apoptotic cells in 7, 21 and 28 d of postnatal life were significantly increased in GDM compared to controls (P<0.01). This study showed that the uncontrolled gestational diabetes significantly increases neuronal apoptosis in hippocampal and dentate gyrus in rat offspring.

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Neuronal and astroglial alterations in the hippocampus of a mouse model for type 1 diabetes

Cited by 85 publications

References 75 publications

Alteration of Dentate Gyrus Astrocytes in Diabetic Rats: Protective Role of Urtica dioica

Alteration of Dentate Gyrus Astrocytes in Diabetic Rats: Protective Role of Urtica dioica

Regulation of Structural Plasticity and Neurogenesis during Stress and Diabetes; Protective Effects of Glucocorticoid Receptor Antagonists

Hippocampal Neuronal Apoptosis in Rat Offspring Due to Gestational Diabetes

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