The rise of plasma ACTH induced by ether is mediated through neural pathways entering the medial basal hypothalamus

1980 ◽  
Vol 93 (2) ◽  
pp. 129-133 ◽  
Author(s):  
M. Kárteszi ◽  
G. B. Makara ◽  
E. Stark

Abstract. The effect of ether stress on the release of immunoreactive ACTH was studied in rats with an antero-lateral cut around the medial basal hypothalamus. Ether failed to raise the plasma ACTH level of rats in which an antero-lateral hypothalamic cut and adrenalectomy had been performed 7 to 8 days previously. Plasma ACTH was also unchanged in rats exposed to ether 2 h after an antero-lateral cut. These data suggest that intact neural pathways entering the medial basal hypothalamus from the antero-lateral direction are necessary for the ACTH releasing action of ether stress.

1981 ◽  
Vol 240 (4) ◽  
pp. E441-E446 ◽  
Author(s):  
G. B. Makara ◽  
E. Stark ◽  
M. Karteszi ◽  
M. Palkovits ◽  
G. Rappay

The effects of destroying the paraventricular nucleus (PVN) of the rat hypothalamus on pituitary-adrenal function were studied. Four days after PVN lesions were placed with a rotating knife, the basal plasma corticosterone level was normal, but the corticosterone response to electrical stimulation of the medial basal hypothalamus, surgical trauma, and ether-venesection stress was significantly inhibited. Four and 8 days after PVN lesioning and adrenalectomy, the basal plasma ACTH level was lower, and the rise of plasma ACTH level elicited by a 3-min ether inhalation was significantly smaller than in the adrenalectomized controls. Corticotropin-releasing factor (CRF) activity in the stalk-median eminence extracts from PVN-lesioned rats was significantly less than in the control extracts. The weight of the adrenals was decreased by both 2 and 4 wk after PVN destruction, and 2 wk after hemiadrenalectomy, the compensatory adrenal hypertrophy was inhibited. The plasma corticosterone response to ether-venesection stress was inhibited only temporarily because it returned to normal by the end of the 4th postoperative week. The results are consistent with the hypothesis that a substantial portion of CRF-containing fibers in the stalk-median eminence region either originate from or run though the PVN or its immediate vicinity.


2004 ◽  
Vol 80 (4) ◽  
pp. 481-488 ◽  
Author(s):  
Toshihiro Nakashima ◽  
Mariko Akamatsu ◽  
Akikazu Hatanaka ◽  
Toshikazu Kiyohara

1996 ◽  
Vol 19 (9) ◽  
pp. 1244-1246 ◽  
Author(s):  
Kenji YAMADA ◽  
Takeharu MIURA ◽  
Yoshihiro MIMAKI ◽  
Yutaka SASHIDA

1983 ◽  
Vol 95 (3) ◽  
pp. 351-353 ◽  
Author(s):  
S. B. Seredenin ◽  
Yu. A. Blednov ◽  
B. A. Badyshtov ◽  
N. M. Shevchenko

2004 ◽  
Vol 286 (3) ◽  
pp. R484-R490 ◽  
Author(s):  
Tsuyoshi Saito ◽  
Hideaki Soya

Running becomes a stress, termed running stress, if it persists above the lactate threshold (LT) and results in enhanced plasma ACTH level in humans. Although the exact underlying regulation mechanism is still uncertain, hypothalamic AVP has been shown to play a dominant role in running-induced ACTH release. It is still not known, however, whether running stress activates the hypothalamic AVP-containing neurons that are involved in the activation of the ACTH response. For this reason, we applied our rat running stress model, in which both plasma ACTH and osmolality levels increase just above LT running (supra-LT running), to delineate which hypothalamic AVP neurons were responsive to running stress. Rats were previously habituated to running and then subjected to a 30-min run either just below or above the LT. Plasma samples were collected from these animals to determine ACTH and osmolality levels. Brains were prepared for immunocytochemistry for both AVP/Fos in the hypothalamus and enzyme immunoassay for the stalk median eminence (SME) AVP content. Only supra-LT running resulted in an increase in the number of Fos/AVP-immunoreactive neurons in both the parvocellular paraventricular nucleus (pPVN) and the magnocellular supraoptic nucleus (SON) accompanied by increased ACTH and plasma osmolality levels. Similarly, running reduced the SME content of the AVP. We thus found that AVP-containing neurons located in both the pPVN and SON are responsive to running stress just above the LT.


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