Glial fibrillary acidic protein mRNA levels in the cingulate cortex of individuals with depression, bipolar disorder and schizophrenia

Neuroscience ◽  
2005 ◽  
Vol 133 (2) ◽  
pp. 453-461 ◽  
Author(s):  
M.J. Webster ◽  
J. O’Grady ◽  
J.E. Kleinman ◽  
C.S. Weickert
Endocrinology ◽  
2013 ◽  
Vol 154 (7) ◽  
pp. 2318-2330 ◽  
Author(s):  
Esther Fuente-Martín ◽  
Cristina García-Cáceres ◽  
Francisca Díaz ◽  
Pilar Argente-Arizón ◽  
Miram Granado ◽  
...  

Abstract Hypothalamic inflammation and gliosis are proposed to participate in the pathogenesis of high-fat diet-induced obesity. Because other factors and nutrients also induce weight gain and adiposity, we analyzed the inflammatory and glial responses to a sucrose (S)-enriched diet. Neonatal overnutrition (NON) exacerbates weight gain in response to metabolic challenges; thus, we compared the inflammatory response of male Wistar rats with NON (4 pups/litter) and controls (12 pups/litter) to increased S intake. At weaning rats received water or a 33% sucrose solution and normal chow ad libitum for 2 months. Sucrose increased serum IL-1β and -6 and hypothalamic IL-6 mRNA levels in NON and TNFα mRNA levels in control and NON rats, whereas NON alone had no effect. The astrocyte marker glial fibrillary acidic protein was increased by NON but decreased by S. This was associated with hypothalamic nuclei specific changes in glial fibrillary acidic protein-positive cell number and morphology. Sucrose increased the number of microglia and phosphorylation of inhibitor of -κB and c-Jun N-terminal kinase in control but not NON rats, with no effect on microglia activation markers. Proteins highly expressed in astrocytes (glutamate, glucose, and lactate transporters) were increased by NON but not S, with no increase in vimentin expression in astrocytes, further suggesting that S-induced adiposity is not associated with hypothalamic astrogliosis. Hence, activation of hypothalamic inflammatory processes and gliosis depend not only on weight gain but also on the diet inducing this weight gain and the early nutritional status. These diverse inflammatory processes could indicate a differential disposition to obesity-induced pathologies.


Glia ◽  
1991 ◽  
Vol 4 (6) ◽  
pp. 572-579 ◽  
Author(s):  
Nishi Sharma ◽  
Kathleen Norman-O'guin ◽  
Bridget Shafit-Zagardo

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Xiu-Fang Ding ◽  
Yan Liu ◽  
Zhi-Yi Yan ◽  
Xiao-Juan Li ◽  
Qing-Yu Ma ◽  
...  

The research has only yielded a partial comprehension of MDD and the mechanisms underlying the antidepressant-like effects of XYS. Therefore, in this study, we aimed to explore the effects of XYS on chronic unpredictable mild stress- (CUMS-) induced changes in the neuronal and the astrocytic markers in the mouse hippocampus. The physical states and depressive-like behaviors in mice with CUMS were recorded. The serum contents of brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) were measured. The protein and mRNA expressions and the immunoreactivities of glial fibrillary acidic protein (GFAP) and neuronal nuclei (NeuN) in mouse hippocampus were detected using a Western blot, qRT-PCR, and immunohistochemical staining, respectively. XYS treatment markedly improved the physical state and depressive-like behaviors in mice subjected to CUMS compared with the model group, and the serum contents of BDNF and GDNF were significantly upregulated. XYS treatment also elevated the protein and mRNA levels, as well as the immunoreactivity of GFAP in the hippocampus. However, CUMS did not influence NeuN expression. In conclusion, these results reveal that chronic administration of XYS elicits antidepressant-like effects in a mouse model of depression and may normalize glial fibrillary acidic protein expression in the hippocampi of mice with CUMS.


2010 ◽  
Vol 112 (4) ◽  
pp. 392-401 ◽  
Author(s):  
Uraporn Vongvatcharanon ◽  
Sirirak Mukem ◽  
Wandee Udomuksorn ◽  
Ekkasit Kumarsit ◽  
Surapong Vongvatcharanon

Pathology ◽  
1983 ◽  
Vol 15 (4) ◽  
pp. 373-378 ◽  
Author(s):  
Stephen J. Lolait ◽  
J.H. Harmer ◽  
G. Auteri ◽  
J.S. Pedersen ◽  
B.H. Toh

1992 ◽  
Vol 267 (32) ◽  
pp. 23269-23274
Author(s):  
Y Nakamura ◽  
M Takeda ◽  
S Aimoto ◽  
H Hojo ◽  
T Takao ◽  
...  

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