73. Cell type-specific interleukin-1 receptor 1 mediates distinct downstream effects in the central nervous system following an intracerebralventricular injection of interleukin-1 beta

2014 ◽  
Vol 40 ◽  
pp. e22
Author(s):  
X. Liu ◽  
Q. Chen ◽  
V. Coppola ◽  
N. Quan ◽  
J. Zuo
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Cell Type ◽  
Downstream Effects ◽  
The Central Nervous System ◽  
Cell Type Specific

Effect of a central CRF antagonist on cardiovascular and thermoregulatory responses induced by stress or IL-1 beta

1993 ◽  
Vol 265 (4) ◽  
pp. R834-R839 ◽  
Author(s):  
T. Nakamori ◽  
A. Morimoto ◽  
N. Murakami
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Interleukin 1 ◽  
Corticotropin Releasing Factor ◽  
Mild Stress ◽  
Induced Responses ◽  
Interleukin 1 Beta ◽  
The Central Nervous System ◽  
Beta 2

We investigated the role of central corticotropin-releasing factor (CRF) in the development of cardiovascular and thermal responses induced by stress or by interleukin-1 beta (IL-1 beta) in free-moving rats. Intracerebroventricular (icv) injection of alpha-helical CRF9-41 (10 micrograms), a CRF receptor antagonist, significantly attenuated hypertension, tachycardia, and a rise in body temperature induced by cage-switch stress, a mild stress. However, icv injection of alpha-helical CRF9-41 (10 micrograms) had no effect on hypertension, tachycardia, or fever induced by intraperitoneal (ip) injection of IL-1 beta (2 micrograms/kg) or icv prostaglandin E2 (PGE2, 100 ng). In contrast, icv injection of alpha-helical CRF9-41 (10 micrograms) significantly attenuated hypertension, tachycardia, or fever induced by icv injection of IL-1 beta (20 ng). The present results suggest that central CRF has an important role in the development of the cage-switch stress-induced responses, but it does not seem to contribute to the hypertension, tachycardia, and fever induced by ip IL-1 beta or by central PGE2. However, it is possible that when IL-1 beta directly acts on the central nervous system, some of its actions are mediated by central CRF.

Cell-type specific expression of gangliosides in the central nervous system

1997 ◽  
Vol 69 (9) ◽  
pp. 1903-1910 ◽  
Author(s):  
T. Tai ◽  
Ikuo Kawashima ◽  
H. Ozawa ◽  
Masaharu Kotani ◽  
K. Ogura
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cell Type ◽  
Specific Expression ◽  
Cell Type Specific Expression ◽  
The Central Nervous System ◽  
Cell Type Specific

scholarly journals Induction of interleukin-1 in glia, and its significance in the central nervous system.

1994 ◽  
Vol 64 ◽  
pp. 59
Author(s):  
Yasuko Tomozawa ◽  
Masabumi Minami ◽  
Kazuki Yabuuchi ◽  
Masamichi Satoh
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Interleukin 1 ◽  
The Central Nervous System

scholarly journals Adiponectin Controls Nutrient Availability in Hypothalamic Astrocytes

2021 ◽  
Vol 22 (4) ◽  
pp. 1587
Author(s):  
Nuri Song ◽  
Da Yeon Jeong ◽  
Thai Hien Tu ◽  
Byong Seo Park ◽  
Hye Rim Yang ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adipose Tissue ◽  
Nutrient Availability ◽  
Acid Oxidation ◽  
Cell Type ◽  
Metabolic Processes ◽  
Nutrient Metabolism ◽  
Peripheral Tissues ◽  
The Central Nervous System

Adiponectin, an adipose tissue-derived hormone, plays integral roles in lipid and glucose metabolism in peripheral tissues, such as the skeletal muscle, adipose tissue, and liver. Moreover, it has also been shown to have an impact on metabolic processes in the central nervous system. Astrocytes comprise the most abundant cell type in the central nervous system and actively participate in metabolic processes between blood vessels and neurons. However, the ability of adiponectin to control nutrient metabolism in astrocytes has not yet been fully elucidated. In this study, we investigated the effects of adiponectin on multiple metabolic processes in hypothalamic astrocytes. Adiponectin enhanced glucose uptake, glycolytic processes and fatty acid oxidation in cultured primary hypothalamic astrocytes. In line with these findings, we also found that adiponectin treatment effectively enhanced synthesis and release of monocarboxylates. Overall, these data suggested that adiponectin triggers catabolic processes in astrocytes, thereby enhancing nutrient availability in the hypothalamus.

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