Congenital Iodine Deficiency and Hypothyroidism Impair LTP and Decrease C- and C- Expression in Rat Hippocampus

Dong, Jing; Yin, Huaizhi; Liu, Wanyang; Wang, Ping; Jiang, Ying; Chen, Jie

doi:10.1016/j.neuro.2005.03.003

Cited by 87 publications

(90 citation statements)

References 37 publications

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“…A few previous studies investigated the deleterious effects of thyroid hormone deficiency on the developing hippocampus (HC) (Gould, et al 1991,Lauder & Mugnaini, 1977,1980Rabie et al, 1979;Rami & Rabie, 1988;Rami et al, 1986a,b). Recently several molecular and functional studies have also appeared (Alvarez- Dolado et al, 2001;Alzoubi et al, 2005;Ambrogini et al, 2005;Desouza et al, 2005;Dong et al, 2005;Gerges & Alkadhi, 2004,Gilbert, 2004Gilbert & Paczkowski, 2003;Martinez et al, 2001;Matos, et al 2002;Meaney et al, 2000;Roskoden et al, 1999;Sui & Gilbert, 2003;Uchida et al, 2005;Vaidya et al, 2001;Vara et al, 2002Vara et al, ,2003.…”

Section: Introductionmentioning

confidence: 99%

Novel two-dimensional morphometric maps and quantitative analysis reveal marked growth and structural recovery of the rat hippocampal regions from early hypothyroid retardation

Farahvar

Meisami

2007

Experimental Neurology

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Effects of postnatal hypothyroidism and recovery from this condition on regional growth of the rat hippocampus (HC) were studied using two-dimensional (2D) foldout, morphometric maps of HC and its constituent CA1-CA4 regions. The maps were derived from unfolding serial coronal sections of the rat forebrain, consisting of the entire rostrocaudal extent of HC pyramidal cell layer in the normal control and hypothyroid weanling (P25, postnatal day 25) and young adult (P90) male rats, as well as animals allowed to recover from hypothyroid-induced growth retardation at weaning. The maps revealed novel views of HC regions for assessment of topological relationships and measurement of surface areas of the HC cortical sheet (pyramidal cell layer). In normal control P90 rats, the unfolded HC on each side extended 4 times more laterally than rostrocaudally; total HC surface area was about 40 mm 2 , compared to 30 mm 2 in the weanling, indicating 35% growth from P25 to P90; CA1 took up 52% of the total HC surface area, followed by CA3 (31%) and CA2 and CA4, 8% each. Hypothyroidism resulted in significant (p<0.01) 11% and 20% reductions in the HC surface area in P25 and P90 rats respectively; CA1 and CA4 regions suffered the most reductions while CA3 and CA2 regions the least. Recovering rats examined at P90, exhibited remarkable growth plasticity and recovery in HC regions, as evident by their near normal HC cortical surface area values, compared to age-matched controls. The 2-D maps also revealed growth deficits in all HC regions of the hypothyroid rats; recovery in these parameters occurred across all dimensions, although the anterior-posterior growth was more severely affected than the mediolateral one. These results are confirmed and extended by volumetric analysis of laminar volumes of HC regions presented in a companion paper (Farahvar et al., 2006). These results imply that HC regions, in contrast to whole brain, possess exceptional growth plasticity, as shown by ability to dramatically recover from early hypothyroid retardation; also 2D morphometric maps are useful tools to visualize complex and convoluted regional sheet of HC cortex and depict quantitative aspects of growth in normal and experimental conditions.

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Section: Introductionmentioning

confidence: 99%

Novel two-dimensional morphometric maps and quantitative analysis reveal marked growth and structural recovery of the rat hippocampal regions from early hypothyroid retardation

Farahvar

Meisami

2007

Experimental Neurology

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“…The total integrated optical density (IOD), a parameter representing the expression levels of FABP1 and gastrin R in the testicular tissue, was determined using a Bx41 cast-grid microscope with DP10 camera (Olympus, Tokyo, Japan) together with an image-analysis program (MetaMorph offline, version 4.65; Molecular Devices, Sunnyvale, CA, USA). Under a magnification of x200, five images were examined in each immunostained section and the average IOD was calculated (15)(16)(17).…”

Section: Methodsmentioning

confidence: 99%

Changes in FABP1 and gastrin receptor expression in the testes of rats that have undergone electrical injury

Huang

Liu

2015

Experimental and Therapeutic Medicine

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Abstract. Testicular trauma may occur due to accidental electrical injury. The aim of this study was to investigate alterations in the levels of fatty acid-binding protein 1 (FABP1) and gastrin receptor (gastrin R) in the testes following electrical injury. Sprague-Dawley rats were divided into control, fatal electrocution (220 V, 50 Hz, 60 sec) and electrical injury (220 V, 50 Hz, 60 sec) groups (n=8 per group). The animals in the fatal electrocution and electrical injury groups were deeply anesthetized with sodium pentobarbital prior to each treatment, in which the current was delivered via an anode connected to the left foreleg and a cathode to the right hindleg. The rats that survived were subsequently sacrificed by cervical dislocation. Control animals received cervical dislocation alone. Immunohistochemical analysis was performed to evaluate the protein expression of FABP1 and gastrin R in the testes. Sections were evaluated by digital image analysis. The expression levels of FABP1 and gastrin R were significantly increased following electrical injury, supported by an increase in the integrated optical density (IOD) when compared with that in the control group (P<0.05). However, no significant difference was found in FABP1 and gastrin R expression levels between the fatal electrocution and control groups. In summary, the protein expression levels of FABP1 and gastrin R were found to be significantly altered by electrical injury, suggesting that these two proteins may be important in underlying mechanisms of testicular injury during electrical injury. The findings indicate that such alterations would be reflected in abnormal testicular function.

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“…After washing, tissue sections were incubated for 10 min in streptavidin-peroxidase and then washed three more times in PBS. Positive signals were visualized with diaminobenzidine, followed by counter-staining with methyl green as previously described (17)(18)(19). PBS was substituted for the primary antibody for the negative control.…”

Section: Methodsmentioning

confidence: 99%

“…Total integrated optical density (IOD), a parameter representing the expression levels of enolase and cav-1 in cardiac tissue, was determined using a cast-grid microscope (MetaMorph/DP10/Bx41, UIC/Olympus, US/JP) together with an image-analysis program (MetaMorph offline, version 4.65). Under magnification of x400, five images were captured for each immunostained section and the average IOD value was calculated as previously described (18,19).…”

Section: Methodsmentioning

confidence: 99%

Elevated enolase and caveolin-1 in the heart of rats following dexamethasone-induced toxicity

Huang

Liu

2012

Mol Med Report

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Abstract. Dexamethasone (DEX)-induced heart damage is associated with enzyme and protein alterations. The purpose of this study was to investigate DEX-induced alterations in cardiac enolase and caveolin-1 (cav-1) following DEX administration. Male Wistar rats were randomly divided into two groups: a control and a DEX. The DEX group intraperitoneally received DEX at the single dose of 10 mg/kg for 7 consecutive days, and the control was given the same amount of saline via the same route. On day 8, the rats were anesthetized, and a thoracotomy was performed in all animals. Immunohistochemical analysis was performed to evaluate protein expression of enolase and cav-1. Sections were analyzed by digital image analysis. Our results demonstrated that cardiac protein expression of enolase and cav-1 was altered following DEX-induced toxicity in the rat. The expression of enolase and cav-1 was significantly increased after DEX treatment, supported by integrated optical density compared with the control (P<0.05). In conclusion, following DEX-induced toxicity, protein expression of enolase and cav-1 was significantly elevated. The current findings indicate that such alterations would be reflected in abnormal cardiac function, and the proteins identified in this study may be useful in revealing the mechanisms underlying DEX-induced toxicity and also in providing various clues for further research.

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Congenital Iodine Deficiency and Hypothyroidism Impair LTP and Decrease C- and C- Expression in Rat Hippocampus

Cited by 87 publications

References 37 publications

Novel two-dimensional morphometric maps and quantitative analysis reveal marked growth and structural recovery of the rat hippocampal regions from early hypothyroid retardation

Novel two-dimensional morphometric maps and quantitative analysis reveal marked growth and structural recovery of the rat hippocampal regions from early hypothyroid retardation

Changes in FABP1 and gastrin receptor expression in the testes of rats that have undergone electrical injury

Elevated enolase and caveolin-1 in the heart of rats following dexamethasone-induced toxicity

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