Alteration in dendritic morphology of cortical neurons in rats with diabetes mellitus induced by streptozotocin

Martínez-Téllez, Rubelia Isaura; Gómez-Villalobos, Ma De Jesús; Flores, Gonzalo

doi:10.1016/j.brainres.2005.04.048

Cited by 105 publications

(86 citation statements)

References 73 publications

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“…Previous studies have indicated that levels of chronic hyperglycemia similar to those achieved in our model cause morphological/biochemical changes that appear to differentially affect the cortex compared with the hippocampus. Specifically, STZ diabetes preferentially decreases dendritic neuronal length in the cortex compared with the hippocampus (28). Additionally, the induction of STZ diabetes alters neuronal cell density differently in the hippocampus compared with the cortex (27).…”

Section: Discussionmentioning

confidence: 95%

Diabetes increases brain damage caused by severe hypoglycemia

Bree¹,

Tejera²,

Daphna-Iken³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

112

105

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Bree AJ, Puente EC, Daphna-Iken D, Fisher SJ. Diabetes increases brain damage caused by severe hypoglycemia. Am J Physiol Endocrinol Metab 297: E194 -E201, 2009. First published May 12, 2009 doi:10.1152/ajpendo.91041.2008.-Insulin-induced severe hypoglycemia causes brain damage. The hypothesis to be tested was that diabetes portends to more extensive brain tissue damage following an episode of severe hypoglycemia. Nine-week-old male streptozotocin-diabetic (DIAB; n ϭ 10) or vehicle-injected control (CONT; n ϭ 7) SpragueDawley rats were subjected to hyperinsulinemic (0.2 U⅐kg Ϫ1 ⅐min Ϫ1 ) severe hypoglycemic (10 -15 mg/dl) clamps while awake and unrestrained. Groups were precisely matched for depth and duration (1 h) of severe hypoglycemia (CONT 11 Ϯ 0.5 and DIAB 12 Ϯ 0.2 mg/dl, P ϭ not significant). During severe hypoglycemia, an equal number of episodes of seizure-like activity were noted in both groups. One week later, histological analysis demonstrated extensive neuronal damage in regions of the hippocampus, especially in the dentate gyrus and CA1 regions and less so in the CA3 region (P Ͻ 0.05), although total hippocampal damage was not different between groups. However, in the cortex, DIAB rats had significantly (2.3-fold) more dead neurons than CONT rats (P Ͻ 0.05). There was a strong correlation between neuronal damage and the occurrence of seizure-like activity (r 2 Ͼ 0.9). Separate studies conducted in groups of diabetic (n ϭ 5) and nondiabetic (n ϭ 5) rats not exposed to severe hypoglycemia showed no brain damage. In summary, under the conditions studied, severe hypoglycemia causes brain damage in the cortex and regions within the hippocampus, and the extent of damage is closely correlated to the presence of seizure-like activity in nonanesthetized rats. It is concluded that, in response to insulin-induced severe hypoglycemia, diabetes uniquely increases the vulnerability of specific brain areas to neuronal damage.Fluoro-Jade; insulin; seizure; streptozotocin HYPOGLYCEMIA IS THE MOST PREVALENT clinical complication in the daily management of insulin-treated people with diabetes, and hypoglycemia continues to be the limiting factor in the glycemic management of diabetes (15). Since severe hypoglycemia affects 40% of insulin-treated people with diabetes (49), concern regarding the hazardous potential for severe hypoglycemia to cause "brain damage" continues to be a very real barrier in striving to fully realize the benefits associated with intensive glycemic control (14). Animal models have unambiguously demonstrated that acute episodes of severe hypoglycemia [blood glucose (BG) Ͻ18 mg/dl] reproducibly induce neuronal damage, especially in the vulnerable neurons in the cortex and hippocampus (2,9,33,44,45,54). Deficits in learning and memory have been shown to be a direct consequence of this severe hypoglycemia-induced hippocampal neuronal damage (2,44,45). However, clincial studies in patients with diabetes have yielded variable results, since episodes of severe hypoglycemia have been shown to alter br...

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Section: Discussionmentioning

confidence: 95%

Diabetes increases brain damage caused by severe hypoglycemia

Bree¹,

Tejera²,

Daphna-Iken³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

112

105

View full text Add to dashboard Cite

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“…Esto puede afectar la integración sináptica y la neurotransmisión (5,6). Se requiere ensayar otras fórmulas de impregnación argéntica, como la versión más reciente del método de Golgi-Cox (30), para incrementar la cantidad de neuronas impregnadas, y acudir a métodos que permitan evaluar cuantitativamente las modificaciones de la arborización dendrítica, tales como el método de Sholl, utilizado en estudios recientes (31)(32)(33). Lo anterior combinado con el análisis de la expresión de proteínas del citoesqueleto (MAP-2, NF y otras) contribuirán a determinar qué tan importante puede ser la patología dendrítica como componente de la patogénesis de la rabia.…”

Section: Discussionunclassified

Alteraciones de la morfología dendrítica neuronal en la corteza cerebral de ratones infectados con rabia: un estudio con la técnica de Golgi

2007

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Introducción. Los signos neurológicos de la rabia son impresionantes; no obstante, el cerebro infectado sufre apenas cambios histológicos muy sutiles. Objetivo. Estudiar la morfología neuronal mediante la técnica de Golgi, en la corteza cerebral de ratones infectados con el virus de la rabia. Materiales y métodos. Se inocularon ratones con virus silvestre de la rabia (virus 'calle') de origen canino o con virus adaptado (virus 'fijo') de la cepa CVS (challenge virus standard). Los animales se sacrificaron en la fase terminal de la enfermedad y se fijaron por perfusión con paraformaldehído. Los cerebros se procesaron con la técnica de Golgi, se obtuvieron cortes coronales de la corteza, se contaron las neuronas impregnadas en un área de 1 mm 2 , se midió el tamaño de sus cuerpos celulares y se tomaron fotografías en diferentes planos de profundidad. Resultados. Se observaron alteraciones morfológicas notables en el soma y las dendritas de neuronas piramidales, con pérdida acentuada de espinas, en 12,9% de neuronas corticales de animales infectados con virus 'calle' por vía intracerebral; en 8,2% de neuronas de ratones inoculados con este mismo virus por la ruta intramuscular y en 31,8% de neuronas en los animales inoculados con virus 'fijo' por vía intramuscular. Además, en las muestras de material infectado el número de neuronas impregnadas por la técnica de Golgi fue considerablemente menor al observado en las muestras no infectadas. Conclusiones. Estos resultados son evidencia de que el virus de la rabia sí puede inducir daño neuronal estructural. Además, esta infección aparentemente interfiere con los mecanismos de impregnación argéntica del método de Golgi.Palabras clave: rabia, virus de la rabia, corteza cerebral, neuronas, neuroanatomía, técnicas histológicas. Neuronal dentritic morphology alterations in the cerebral cortex of rabies-infected mice: a Golgi studyIntroduction. The neurological signs of rabies are very dramatic. Nevertheless, the infected brain manifests only very subtle histological changes. Objective. The neuronal morphology in the cerebral cortex of rabies-infected mice was examined by means the Golgi technique for detection of neuropathy. Materials and methods. Two groups of mice were inoculated with rabies-one with street virus isolated from an infected dog and the second with fixed CVS (challenge virus standard) virus. At the terminal phase of illness, the animals were sacrificed and fixed for histological staining by perfusion with paraformaldehyde. Next, the brains were treated by the Golgi technique and coronal sections were obtained. Neurons enclosed within 1 mm 2 frames of the frontal cortex sections were counted and the sizes of the cellular bodies were measured. Photographs of several depth levels from the sections were obtained. Results. Cortical pyramidal neurons showed distinctive morphological alterations in the soma and dendrites (including loss of dendritic spines) in 12.9% of cells from intracerebral infectedmice with street virus; in 8.2% of neurons from intramuscular inf...

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“…[5,7] Findings of the research and evidences in the literature revealed reduced neurogenesis in the dentate gyrus of diabetic hippocampus [8] and decreased dendritic arborization. [9] Stress exposure triggered fear memory and anxiety, and decreased the hippocampal-dependent memory performance in mice. [10,11] Numerous studies revealed that the stress exposure causes alterations in synaptic function and plasticity [12] in dendritic remodeling of hippocampal neurons.…”

Section: What This Study Adds To the Fieldmentioning

confidence: 99%

Effect of environmental enrichment exposure on neuronal morphology of streptozotocin-induced diabetic and stressed rat hippocampus

Pamidi¹,

Nayak²

2014

Biomed J

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Background: Environmental enrichment (EE) exposure is known to influence the structural changes in the neuronal network of hippocampus. In the present study, we evaluated the effects of EE exposure on the streptozotocin (STZ)-induced diabetic and stressed rat hippocampus. Methods:Male albino rats of Wistar strain (4-5 weeks old) were grouped into normal control (NC), vehicle control (VC), diabetes (DI), diabetes + stress (DI + S), diabetes + EE (DI + E), and diabetes + stress + EE (DI + S + E) groups (n = 8 in each group). Rats were exposed to stress and EE after inducing diabetes with STZ (40 mg/kg). Rats were sacrificed on Day 30 and brain sections were processed for cresyl violet staining to quantify the number of surviving neurons in the CA1, CA3, and dentate hilus (DH) regions of hippocampus. Results:A significant (p < 0.001) decrease in the number of survived neurons was noticed in DI (CA1, 34.06 ± 3.2; CA3, 36.1 ± 3.62; DH, 9.83 ± 2.02) as well as DI + S (CA1, 14.03 ± 3.12; CA3, 20.27 ± 4.09; DH, 6.4 ± 1.21) group rats compared to NC rats (CA1, 53.64 ± 2.96; CA3, 62.1 ± 3.34; DH, 21.11 ± 1.03). A significant (p < 0.001) increase in the number of survived neurons was observed in DI + E (CA1, 42.3 ± 3.66; CA3, 46.73 ± 4.74; DH, 17.03 ± 2.19) and DI + S + E (CA1 , 29.69 ± 4.47; CA3, 36.73 ± 3.89; DH, 12.23 ± 2.36) group rats compared to DI and DI + S groups, respectively. Conclusions: EE exposure significantly reduced the amount of neuronal damage caused by complications of diabetes and stress to the neurons of hippocampus. (Biomed J 2014;37:225-231)

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Alteration in dendritic morphology of cortical neurons in rats with diabetes mellitus induced by streptozotocin

Cited by 105 publications

References 73 publications

Diabetes increases brain damage caused by severe hypoglycemia

Diabetes increases brain damage caused by severe hypoglycemia

Alteraciones de la morfología dendrítica neuronal en la corteza cerebral de ratones infectados con rabia: un estudio con la técnica de Golgi

Effect of environmental enrichment exposure on neuronal morphology of streptozotocin-induced diabetic and stressed rat hippocampus

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