Effects of Intravenous Administration of Interleukin-1-Beta on the Release of Prostaglandin E2, Corticotropin-Releasing Factor, and Arginine Vasopressin in Several Hypothalamic Areas of Freely Moving Rats: Estimation by Push-Pull Perfusion

1994 ◽  
Vol 60 (1) ◽  
pp. 8-15 ◽  
Author(s):  
Hajime Watanobe ◽  
Kazuo Takebe
1993 ◽  
Vol 265 (4) ◽  
pp. R834-R839 ◽  
Author(s):  
T. Nakamori ◽  
A. Morimoto ◽  
N. Murakami

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.


1990 ◽  
Vol 258 (1) ◽  
pp. E163-E171 ◽  
Author(s):  
G. Katsuura ◽  
A. Arimura ◽  
K. Koves ◽  
P. E. Gottschall

Intravenous administration of recombinant human interleukin 1 beta (IL-1 beta, 1 micrograms/100 g body wt) resulted in a marked elevation of plasma adrenocorticotropic hormone (ACTH) levels, with peak levels at 10 min, in conscious unrestrained rats. One week after the placement of a lesion by radiofrequency or microinjection of kainic acid in the organum vasculosum of lamina terminalis (OVLT) but not in subfornical organ, ACTH response to intravenous IL-1 beta was enhanced, whereas both radiofrequency-induced lesion and kainic acid in the preoptic area (POA) suppressed the response. Indomethacin or a prostaglandin E (PGE) antagonist microinjected into the OVLT or POA suppressed or abolished the response. On the other hand, PGE, but not PGD2, microinjected into the POA increased plasma ACTH levels. These results suggest an important role for the OVLT, which lacks blood-brain barrier, as a possible site of entry of blood-borne IL-1 beta into the brain and for the POA, which may contain the neurons required for the response. Involvement of PGE in the OVLT and POA in the ACTH response to intravenous IL-1 beta is also suggested.


1991 ◽  
Vol 192 (1) ◽  
pp. 185-187 ◽  
Author(s):  
Akira Uehara ◽  
Toshikatsu Okumura ◽  
Yasutaka Kumei ◽  
Yuichi Takasugi ◽  
Masayoshi Namiki

1993 ◽  
Vol 623 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Ryuichi Takahata ◽  
Hitoshi Matsumura ◽  
Sachi Sri Kantha ◽  
Etsuko Kubo ◽  
Kumiko Kawase ◽  
...  

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